PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 11723253-3 2001 Both agents inhibited the TNF-alpha- or TPA-induced expression of cyclooxygenase (COX)-2 mRNA and protein, COX-2 promoter activity, and prostaglandin E2 (PGE2) production. Dinoprostone 136-152 tumor necrosis factor Homo sapiens 26-35 11723253-3 2001 Both agents inhibited the TNF-alpha- or TPA-induced expression of cyclooxygenase (COX)-2 mRNA and protein, COX-2 promoter activity, and prostaglandin E2 (PGE2) production. Dinoprostone 154-158 tumor necrosis factor Homo sapiens 26-35 11723253-6 2001 These results suggest that the inhibitory effect of GF-015 and GF-90 on TNF-alpha-induced COX-2 protein expression was caused by suppression of IKK activity and NF-kappaB activation in the COX-2 promoter, resulting in attenuation of COX-2 gene expression and PGE2 production. Dinoprostone 259-263 tumor necrosis factor Homo sapiens 72-81 11592370-10 2001 The combination of IL-1beta and TNFalpha had an additive effect on PGE2 production, while addition of IL-17 to TNFalpha or IL-1beta synergistically enhanced PGE2 production. Dinoprostone 67-71 tumor necrosis factor Homo sapiens 32-40 11774822-7 2001 Moreover, the postburn plasma TNF alpha level was negatively correlated to that of PGE2. Dinoprostone 83-87 tumor necrosis factor Homo sapiens 30-39 11774822-9 2001 And PGE2 might down-regulate TNF alpha production. Dinoprostone 4-8 tumor necrosis factor Homo sapiens 29-38 11592370-10 2001 The combination of IL-1beta and TNFalpha had an additive effect on PGE2 production, while addition of IL-17 to TNFalpha or IL-1beta synergistically enhanced PGE2 production. Dinoprostone 157-161 tumor necrosis factor Homo sapiens 111-119 11468174-7 2001 However, the addition of LPS, LTA, LPS plus IFN-gamma, or tumor necrosis factor alpha (TNF-alpha) plus prostaglandin E2 to such cells again resulted in the rapid induction of apoptosis in the majority of cells, together with a reduced production of IL-12 p70 and TNF-alpha. Dinoprostone 103-119 tumor necrosis factor Homo sapiens 263-272 11489969-6 2001 Cyclooxygenase-2 expression and PGE2 release was increased by TPA and TNF-alpha but not by HCMV infection. Dinoprostone 32-36 tumor necrosis factor Homo sapiens 70-79 11369638-3 2001 Here it is reported that prostaglandin E(2) (PGE(2)), an inflammatory mediator with a previously known Th2-driving function, dose-dependently enhances the IL-12p40 mRNA expression and the secretion of IL-12p40 protein in human tumor necrosis factor-alpha (TNFalpha)-stimulated immature dendritic cells (DCs). Dinoprostone 25-43 tumor necrosis factor Homo sapiens 227-254 11570587-6 2001 Our studies on the regulation of IL-10 secretion in OVCAR-3 revealed that (1) proinflammatory stimuli IL-1beta and TNF-alpha, but not LPS, enhance IL-10 secretion, (2) IL-6 has no influence on the release of IL-10, (3) prostaglandin E2 influences neither the spontaneous nor the TNF-alpha- or IL-1beta-stimulated IL-10 production and (4) interferon-gamma inhibits IL-10 secretion. Dinoprostone 219-235 tumor necrosis factor Homo sapiens 115-124 11369638-3 2001 Here it is reported that prostaglandin E(2) (PGE(2)), an inflammatory mediator with a previously known Th2-driving function, dose-dependently enhances the IL-12p40 mRNA expression and the secretion of IL-12p40 protein in human tumor necrosis factor-alpha (TNFalpha)-stimulated immature dendritic cells (DCs). Dinoprostone 25-43 tumor necrosis factor Homo sapiens 256-264 11369638-3 2001 Here it is reported that prostaglandin E(2) (PGE(2)), an inflammatory mediator with a previously known Th2-driving function, dose-dependently enhances the IL-12p40 mRNA expression and the secretion of IL-12p40 protein in human tumor necrosis factor-alpha (TNFalpha)-stimulated immature dendritic cells (DCs). Dinoprostone 45-51 tumor necrosis factor Homo sapiens 227-254 11369638-3 2001 Here it is reported that prostaglandin E(2) (PGE(2)), an inflammatory mediator with a previously known Th2-driving function, dose-dependently enhances the IL-12p40 mRNA expression and the secretion of IL-12p40 protein in human tumor necrosis factor-alpha (TNFalpha)-stimulated immature dendritic cells (DCs). Dinoprostone 45-51 tumor necrosis factor Homo sapiens 256-264 11289153-8 2001 TNF-alpha induction of COX-2 and prostaglandin E2 correlated inversely with induction of apoptosis. Dinoprostone 33-49 tumor necrosis factor Homo sapiens 0-9 11298495-7 2001 Indeed, PGE(2) may exert negative feedback on the release of TNF-alpha. Dinoprostone 8-13 tumor necrosis factor Homo sapiens 61-70 11310848-9 2001 Suppression of TNFalpha-induced MMP-9 secretion by TGF-beta correlated with a reduction in prostaglandin E2 (PGE2) secretion. Dinoprostone 91-107 tumor necrosis factor Homo sapiens 15-23 11310848-9 2001 Suppression of TNFalpha-induced MMP-9 secretion by TGF-beta correlated with a reduction in prostaglandin E2 (PGE2) secretion. Dinoprostone 109-113 tumor necrosis factor Homo sapiens 15-23 11310848-10 2001 Furthermore, the effect of TGF-beta or indomethacin on blockage of TNF-alpha-stimulated MMP-9 production was reversed by the addition of either exogenous PGE2 or the cyclic AMP (cAMP) analogue Bt2cAMP. Dinoprostone 154-158 tumor necrosis factor Homo sapiens 67-76 11310848-11 2001 Thus, we concluded that TGF-beta acts as a potent suppressor of TNF-alpha-induced monocyte MMP-9 synthesis via a PGE2- and cAMP-dependent mechanism. Dinoprostone 113-117 tumor necrosis factor Homo sapiens 64-73 11456350-2 2001 We have previously reported that inflammatory mediators interleukin-1 (IL-1) and tumor necrosis factor alpha (TNFalpha) increase the production of PGE2 in human gingival fibroblasts. Dinoprostone 147-151 tumor necrosis factor Homo sapiens 81-108 11456350-2 2001 We have previously reported that inflammatory mediators interleukin-1 (IL-1) and tumor necrosis factor alpha (TNFalpha) increase the production of PGE2 in human gingival fibroblasts. Dinoprostone 147-151 tumor necrosis factor Homo sapiens 110-118 11487149-6 2001 Concomitant addition of IL-1alpha and PGE2 or TNF-alpha and PGE2 suppressed MMP-1 mRNA production, compared with the groups treated with IL-1alpha or TNF-alpha alone. Dinoprostone 38-42 tumor necrosis factor Homo sapiens 150-159 11250126-3 2001 In this study, of the cytokines that are found at increased levels in AD brain (interleukin (IL)-1alpha, IL-1beta, IL-6 and tumour necrosis factor (TNF)alpha), IL-1beta was found to induce COX-2 immunoreactivity and prostaglandin (PG) E2 secretion by human neuroblastoma cell line SK-N-SH. Dinoprostone 231-237 tumor necrosis factor Homo sapiens 124-157 11487149-6 2001 Concomitant addition of IL-1alpha and PGE2 or TNF-alpha and PGE2 suppressed MMP-1 mRNA production, compared with the groups treated with IL-1alpha or TNF-alpha alone. Dinoprostone 60-64 tumor necrosis factor Homo sapiens 150-159 11487149-7 2001 In contrast, PGE2 enhanced the upregulatory effects of TIMP-1 mRNA by IL-1alpha or TNF-alpha. Dinoprostone 13-17 tumor necrosis factor Homo sapiens 83-92 11158257-5 2001 Localized, but strong, expression of tumor necrosis factor-alpha and interleukin-1ss mRNA was found at the edge of the intracerebroventricular tract, which was largely prevented by the central prostaglandin E2 injection. Dinoprostone 193-209 tumor necrosis factor Homo sapiens 37-64 11305695-9 2001 These data suggest that TNF-alpha potentiates Ang II-induced synthesis of PGI2 and PGE2 in a tyrosine kinase-dependent manner, an effect that may contribute to the counter-regulatory influence of prostaglandins on the pressor effects of Ang II in the vasculature. Dinoprostone 83-87 tumor necrosis factor Homo sapiens 24-33 11216681-13 2001 Exogenous tumor necrosis factor-alpha also enhanced the release of interleukin-6 (p<0.01) and transforming growth factor-beta1 (p<0.05), whereas the secretion of transforming growth factor-beta1 was increased by insulin-like growth factor-I and prostaglandin E2 as well. Dinoprostone 251-267 tumor necrosis factor Homo sapiens 10-37 11158257-7 2001 Although exogenous prostaglandin E2 increased lipopolysaccharide-induced NF-kappaB activity and cyclooxygenase-2 transcription in vascular-associated elements, it significantly reduced microglial activation and tumor necrosis factor-alpha expression in the brain parenchyma. Dinoprostone 19-35 tumor necrosis factor Homo sapiens 211-238 11154420-0 2000 Prostaglandins E2 and I2 downregulate tumor necrosis factor alpha-induced intercellular adhesion molecule-1 expression in human oral gingival epithelial cells. Dinoprostone 0-17 tumor necrosis factor Homo sapiens 38-65 11104733-4 2000 Pretreatment of HASM with prostaglandin (PG) E(2), forskolin, or dibutyryl cAMP inhibited TNF-alpha-induced RANTES secretion but increased TNF-alpha-induced IL-6 secretion. Dinoprostone 26-49 tumor necrosis factor Homo sapiens 90-99 11104733-4 2000 Pretreatment of HASM with prostaglandin (PG) E(2), forskolin, or dibutyryl cAMP inhibited TNF-alpha-induced RANTES secretion but increased TNF-alpha-induced IL-6 secretion. Dinoprostone 26-49 tumor necrosis factor Homo sapiens 139-148 11095928-1 2000 Tumour necrosis factor (TNF)-alpha-stimulated prostaglandin (PG) E(2)biosynthesis by amnion-derived AV3 cells is accompanied by increased prostaglandin H synthase (PGHS)-2 mRNA expression. Dinoprostone 46-69 tumor necrosis factor Homo sapiens 0-34 11154420-8 2000 From these results, we suggest that PGE2 and PGI2 inhibit TNF alpha-elicited ICAM-1 expression by cAMP-dependent pathways via EP4 receptors and IP receptors, respectively. Dinoprostone 36-40 tumor necrosis factor Homo sapiens 58-67 11154420-1 2000 In the present study, we examined whether prostaglandin (PG) E2 and PGI2 regulated intercellular adhesion molecule-1 (ICAM-1) expression in human oral gingival epithelial cells stimulated with tumor necrosis factor alpha (TNF alpha). Dinoprostone 42-63 tumor necrosis factor Homo sapiens 193-220 11154420-1 2000 In the present study, we examined whether prostaglandin (PG) E2 and PGI2 regulated intercellular adhesion molecule-1 (ICAM-1) expression in human oral gingival epithelial cells stimulated with tumor necrosis factor alpha (TNF alpha). Dinoprostone 42-63 tumor necrosis factor Homo sapiens 222-231 11154420-3 2000 PGE2 and carbacyclin (a stable analogue of PGI2) significantly decreased ICAM-1 expression in TNF alpha-challenged oral gingival epithelial cells. Dinoprostone 0-4 tumor necrosis factor Homo sapiens 94-103 10946303-1 2000 TNF-alpha induced a dose- and time-dependent increase in cyclooxygenase-2 (COX-2) expression and PGE2 formation in human NCI-H292 epithelial cells. Dinoprostone 97-101 tumor necrosis factor Homo sapiens 0-9 10946303-11 2000 These results suggest that, in NCI-H292 epithelial cells, TNF-alpha might activate phospholipase C-gamma2 via an upstream tyrosine kinase to induce activation of PKC-alpha and protein tyrosine kinase, resulting in the activation of NF-kappaB-inducing kinase and IKK1/2, and NF-kappaB in the COX-2 promoter, then initiation of COX-2 expression and PGE2 release. Dinoprostone 347-351 tumor necrosis factor Homo sapiens 58-67 10946311-3 2000 At concentrations found in the synovial fluid of RA patients, exogenously added sPLA2-IIA dose-dependently amplified TNF-alpha-stimulated PGE2 production by cultured synovial fibroblasts. Dinoprostone 138-142 tumor necrosis factor Homo sapiens 117-126 10896240-6 2000 Addition of exogenous PGE2 before incubation nearly abrogated the effect of aspirin on TNF-alpha, substantiating the role of PGE2 as a regulator of TNF-alpha synthesis, whereas the effect on FPA was small. Dinoprostone 22-26 tumor necrosis factor Homo sapiens 87-96 10946311-4 2000 Enhancement of TNF-alpha-stimulated PGE2 production in synovial cells was accompanied by increased expression of cyclooxygenase (COX)-2 and cytosolic phospholipase A2 (cPLA2)-alpha. Dinoprostone 36-40 tumor necrosis factor Homo sapiens 15-24 10896240-6 2000 Addition of exogenous PGE2 before incubation nearly abrogated the effect of aspirin on TNF-alpha, substantiating the role of PGE2 as a regulator of TNF-alpha synthesis, whereas the effect on FPA was small. Dinoprostone 22-26 tumor necrosis factor Homo sapiens 148-157 10896240-6 2000 Addition of exogenous PGE2 before incubation nearly abrogated the effect of aspirin on TNF-alpha, substantiating the role of PGE2 as a regulator of TNF-alpha synthesis, whereas the effect on FPA was small. Dinoprostone 125-129 tumor necrosis factor Homo sapiens 148-157 10623427-1 1999 Tumour necrosis factor alpha (TNF-alpha) inflammatory activity is mediated, at least in part, by prostaglandin E(2)(PGE(2)). Dinoprostone 97-115 tumor necrosis factor Homo sapiens 30-39 10783136-1 2000 Normal human lung fibroblasts downregulate the production of tumor necrosis factor (TNF)-alpha by activated monocytes through the production of prostaglandin E(2) (PGE(2)), contributing to the local control of the inflammatory process. Dinoprostone 144-162 tumor necrosis factor Homo sapiens 61-94 10783136-5 2000 We have also observed that the ability of TNF-alpha to induce PGE(2) was impaired in FF and was related to a reduced expression of cyclooxygenase 2. Dinoprostone 62-68 tumor necrosis factor Homo sapiens 42-51 10858012-4 2000 RESULTS: In response to IL-1beta and TNF-alpha combined cells of the thyroid epithelial cell line Nthy-ori3-1 secreted marked amounts of PGE2 in a time-dependent fashion. Dinoprostone 137-141 tumor necrosis factor Homo sapiens 37-46 11193500-6 2000 COX-2 has been focused as a key enzyme to regulate PGE2 synthesis and plays an important role in inflammation, because COX-2 was induced in many types of cells by the stimulation of inflammatory cytokines such as interleukin-1 beta (IL-1 beta) and tumor necrosis factor alpha (TNF alpha). Dinoprostone 51-55 tumor necrosis factor Homo sapiens 248-275 11193500-6 2000 COX-2 has been focused as a key enzyme to regulate PGE2 synthesis and plays an important role in inflammation, because COX-2 was induced in many types of cells by the stimulation of inflammatory cytokines such as interleukin-1 beta (IL-1 beta) and tumor necrosis factor alpha (TNF alpha). Dinoprostone 51-55 tumor necrosis factor Homo sapiens 277-286 10671814-1 2000 The effects of five inflammatory cytokines, i.e. interleukin(IL)-1alpha, IL-1beta, IL-6, IL-8 and tumor necrosis factor-alpha (TNF-alpha) on prostaglandin E(2) (PGE(2)) production from amnion cells cultured in a serum-free condition was evaluated. Dinoprostone 141-159 tumor necrosis factor Homo sapiens 127-136 10674980-0 1999 LPS mediated production of IL-1, PGE2 and PGF2alpha from term decidua involves tumour necrosis factor and tumour necrosis factor receptor p55. Dinoprostone 33-37 tumor necrosis factor Homo sapiens 79-101 10616001-7 1999 Fluoxetine and amitriptyline (0.3 microg/ml, 1 microg/ml, and 3 microg/ml) significantly (P<0.05) inhibited PGE2 release in the media of human synovial cells in the presence of IL-1alpha plus TNFalpha, in a dose-dependent manner (up to 88% inhibition). Dinoprostone 111-115 tumor necrosis factor Homo sapiens 195-203 10674980-0 1999 LPS mediated production of IL-1, PGE2 and PGF2alpha from term decidua involves tumour necrosis factor and tumour necrosis factor receptor p55. Dinoprostone 33-37 tumor necrosis factor Homo sapiens 106-128 10433808-8 1999 PGE(2)(1 microM or 10 nM) reduces marrow stromal cell IL-8 synthesis in response to IL-1alpha or TNF-alpha. Dinoprostone 0-6 tumor necrosis factor Homo sapiens 97-106 10697805-6 1999 11-deoxy-PGE1, a selective EP2/EP4 agonist, inhibited TNF alpha-elicited ICAM-1 expression as potently as PGE2, while butaprost, a selective EP2 agonist, was somewhat less effective than PGE2. Dinoprostone 187-191 tumor necrosis factor Homo sapiens 54-63 10697805-7 1999 AH23848B, an EP4 antagonist, antagonized the inhibitory effect of TNF alpha-elicited ICAM-1 expression by PGE2. Dinoprostone 106-110 tumor necrosis factor Homo sapiens 66-75 10697805-11 1999 From these data, we suggest that PGE2 downregulates TNF alpha-induced ICAM-1 expression in HGF, via EP2 and EP4 receptors by cAMP-dependent signaling pathways, which may result in control of inflammatory and immunological responses in periodontal disease. Dinoprostone 33-37 tumor necrosis factor Homo sapiens 52-61 10697805-2 1999 In the present study, we investigated whether PGE2 regulated intercellular adhesion molecule-1 (ICAM-1) expression in human gingival fibroblasts (HGF) stimulated with tumor necrosis factor-alpha (TNF alpha) and if so, which subtype(s) of PGE2 receptors was involved. Dinoprostone 46-50 tumor necrosis factor Homo sapiens 167-194 10697805-2 1999 In the present study, we investigated whether PGE2 regulated intercellular adhesion molecule-1 (ICAM-1) expression in human gingival fibroblasts (HGF) stimulated with tumor necrosis factor-alpha (TNF alpha) and if so, which subtype(s) of PGE2 receptors was involved. Dinoprostone 46-50 tumor necrosis factor Homo sapiens 196-205 10697805-3 1999 Exogenous addition of PGE2 to HGF inhibited ICAM-1 expression elicited by TNF alpha in a concentration-dependent manner. Dinoprostone 22-26 tumor necrosis factor Homo sapiens 74-83 10697805-4 1999 Treatment of HGF with indomethacin, a cyclo-oxygenase inhibitor, had no effect on TNF alpha-elicited ICAM-1 expression, although indomethacin completely inhibited PGE2 production enhanced by TNF alpha. Dinoprostone 163-167 tumor necrosis factor Homo sapiens 191-200 10419778-8 1999 We conclude that PGE(2)inhibits induced TNF-alpha expression in target cells through an Egr-1/Krox-24 mediated signaling process. Dinoprostone 17-23 tumor necrosis factor Homo sapiens 40-49 10476324-7 1999 TNF-alpha stimulation increased the levels of GM-CSF and PGE2 in epithelial cell supernatants and dexamethasone suppressed the TNF-alpha induced increases. Dinoprostone 57-61 tumor necrosis factor Homo sapiens 0-9 10419778-2 1999 We examined the mechanism by which PGE(2)suppresses the expression of TNF-alpha in human macrophages and synovial fibroblasts. Dinoprostone 35-41 tumor necrosis factor Homo sapiens 70-79 10419778-6 1999 An intact Egr-1/Krox-24 enhancer sequence in the TNF-alpha promoter region was essential for the latter PGE(2)-dependent inhibitory effect as double base substitutions (GC-->TT) in the sequence curtailed promoter response to PGE(2). Dinoprostone 104-110 tumor necrosis factor Homo sapiens 49-58 10395955-3 1999 The lipid mediator prostaglandin E2 (PGE2) markedly reduces in a time- and dose-dependent manner the constitutive and TNF-alpha-induced M-CSF synthesis by bone marrow stromal cells. Dinoprostone 19-35 tumor necrosis factor Homo sapiens 118-127 10395955-3 1999 The lipid mediator prostaglandin E2 (PGE2) markedly reduces in a time- and dose-dependent manner the constitutive and TNF-alpha-induced M-CSF synthesis by bone marrow stromal cells. Dinoprostone 37-41 tumor necrosis factor Homo sapiens 118-127 10468047-8 1999 Finally, GM-CSF incubation in vitro elevated TNFalpha synthesis in normal monocytes and in cells treated with a combination of the anti-inflammatory mediators IL-10, TGFbeta, and PGE2. Dinoprostone 179-183 tumor necrosis factor Homo sapiens 45-53 10207535-4 1999 When the cells were treated simultaneously with benzydamine and the cytokines IL-1 beta or TNF alpha, the agent benzydamine reduced (P < 0.05) the stimulatory effect of IL-1 beta and TNF alpha respectively, on PGE2 and PGI2 production in human gingival fibroblasts. Dinoprostone 213-217 tumor necrosis factor Homo sapiens 91-100 10731102-1 1999 Prostaglandin E2 (PGE2) and cytokines, such as interleukin-6 (IL-6) or tumour necrosis factor a (TNFalpha) can regulate aromatase activity. Dinoprostone 0-16 tumor necrosis factor Homo sapiens 97-105 10329351-7 1999 The inclusion of the cPLA2-specific inhibitor arachidonyl trifluoromethyl ketone (AACOCF3) resulted in a concentration-dependent inhibition of PGE2 biosynthesis in WISH cells treated with TNF-alpha (>95 per cent at 2 microM). Dinoprostone 143-147 tumor necrosis factor Homo sapiens 188-197 10211885-0 1999 Inhibition of tumor necrosis factor alpha-induced prostaglandin E2 production by the antiinflammatory cytokines interleukin-4, interleukin-10, and interleukin-13 in osteoarthritic synovial fibroblasts: distinct targeting in the signaling pathways. Dinoprostone 50-66 tumor necrosis factor Homo sapiens 14-41 10211885-1 1999 OBJECTIVE: To investigate the effects of the antiinflammatory cytokines interleukin-4 (IL-4), IL-10, and IL-13 on tumor necrosis factor alpha (TNFalpha)-induced prostaglandin E2 (PGE2) release in the cellular signaling cascade on human osteoarthritis (OA) synovial fibroblasts. Dinoprostone 161-177 tumor necrosis factor Homo sapiens 114-141 10211885-1 1999 OBJECTIVE: To investigate the effects of the antiinflammatory cytokines interleukin-4 (IL-4), IL-10, and IL-13 on tumor necrosis factor alpha (TNFalpha)-induced prostaglandin E2 (PGE2) release in the cellular signaling cascade on human osteoarthritis (OA) synovial fibroblasts. Dinoprostone 161-177 tumor necrosis factor Homo sapiens 143-151 10211885-1 1999 OBJECTIVE: To investigate the effects of the antiinflammatory cytokines interleukin-4 (IL-4), IL-10, and IL-13 on tumor necrosis factor alpha (TNFalpha)-induced prostaglandin E2 (PGE2) release in the cellular signaling cascade on human osteoarthritis (OA) synovial fibroblasts. Dinoprostone 179-183 tumor necrosis factor Homo sapiens 114-141 10211885-1 1999 OBJECTIVE: To investigate the effects of the antiinflammatory cytokines interleukin-4 (IL-4), IL-10, and IL-13 on tumor necrosis factor alpha (TNFalpha)-induced prostaglandin E2 (PGE2) release in the cellular signaling cascade on human osteoarthritis (OA) synovial fibroblasts. Dinoprostone 179-183 tumor necrosis factor Homo sapiens 143-151 10211885-3 1999 RESULTS: IL-4, IL-10, and IL-13 at 5 ng/ml dramatically reduced TNFalpha-induced PGE2 release by approximately 90% (P < 0.0001). Dinoprostone 81-85 tumor necrosis factor Homo sapiens 64-72 10211885-11 1999 CONCLUSION: The results indicate that these antiinflammatory cytokines reversed the TNFalpha-induced release of PGE2 by OA synovial fibroblasts, by acting at various levels of the TNFa-dependent signaling cascade. Dinoprostone 112-116 tumor necrosis factor Homo sapiens 84-92 10211885-11 1999 CONCLUSION: The results indicate that these antiinflammatory cytokines reversed the TNFalpha-induced release of PGE2 by OA synovial fibroblasts, by acting at various levels of the TNFa-dependent signaling cascade. Dinoprostone 112-116 tumor necrosis factor Homo sapiens 84-88 10207535-4 1999 When the cells were treated simultaneously with benzydamine and the cytokines IL-1 beta or TNF alpha, the agent benzydamine reduced (P < 0.05) the stimulatory effect of IL-1 beta and TNF alpha respectively, on PGE2 and PGI2 production in human gingival fibroblasts. Dinoprostone 213-217 tumor necrosis factor Homo sapiens 186-195 10091607-4 1999 HMC released increased amounts of prostaglandin E2 (PGE2) after treatment with several combinations of IL-1 beta, tumor necrosis factor (TNF)-alpha and/or lipopolysaccharide. Dinoprostone 34-50 tumor necrosis factor Homo sapiens 114-147 10091607-4 1999 HMC released increased amounts of prostaglandin E2 (PGE2) after treatment with several combinations of IL-1 beta, tumor necrosis factor (TNF)-alpha and/or lipopolysaccharide. Dinoprostone 52-56 tumor necrosis factor Homo sapiens 114-147 10091607-6 1999 The accumulation of PGE2 elicited by a combination of IL-1 beta/TNF-alpha correlated closely with the temporal pattern of COX-2 protein expression, which reflected the induction of COX-2 mRNA. Dinoprostone 20-24 tumor necrosis factor Homo sapiens 64-73 10091607-7 1999 IL-13 inhibited IL-1 beta/TNF-alpha-elicited PGE2 production, as well as COX-2 protein and mRNA expression in a concentration-dependent fashion. Dinoprostone 45-49 tumor necrosis factor Homo sapiens 26-35 9880560-3 1999 IL-1, TNF-alpha, IFN-gamma, and exogenous sodium nitroprusside, a nitric oxide donor, all stimulated PGE2 production in a dose-dependent manner. Dinoprostone 101-105 tumor necrosis factor Homo sapiens 6-15 9811056-0 1998 Interleukin-1alpha and tumor necrosis factor alpha synergistically stimulate prostaglandin E2-dependent production of interleukin-11 in rheumatoid synovial fibroblasts. Dinoprostone 77-93 tumor necrosis factor Homo sapiens 23-50 10193778-5 1999 Inhibition of LPS-induced TNF-alpha by the selective PDE4 inhibitor RP73401 was proportionally enhanced with endogenous PGE2 (maximal after 24 h). Dinoprostone 120-124 tumor necrosis factor Homo sapiens 26-35 10408703-6 1999 IL-10 production induced by RCC CM was found to be dependent on TNF-alpha and PGE2 since an anti-TNF-alpha antibody (Ab) inhibited 40-70% of IL-10 production by monocytes, and the combination of anti-TNF-alpha Ab and indomethacin, an inhibitor of PGE2 production, inhibited 80-94% of RCC CM-induced IL-10 production by monocytes. Dinoprostone 78-82 tumor necrosis factor Homo sapiens 97-106 10408703-6 1999 IL-10 production induced by RCC CM was found to be dependent on TNF-alpha and PGE2 since an anti-TNF-alpha antibody (Ab) inhibited 40-70% of IL-10 production by monocytes, and the combination of anti-TNF-alpha Ab and indomethacin, an inhibitor of PGE2 production, inhibited 80-94% of RCC CM-induced IL-10 production by monocytes. Dinoprostone 78-82 tumor necrosis factor Homo sapiens 97-106 9845672-10 1998 Increased production of prostaglandin E2 (PGE2) in response to TNF-alpha and IL-1beta treatment was attenuated by IL-4 pretreatment, by 52% and 72%, respectively. Dinoprostone 24-40 tumor necrosis factor Homo sapiens 63-72 9845672-10 1998 Increased production of prostaglandin E2 (PGE2) in response to TNF-alpha and IL-1beta treatment was attenuated by IL-4 pretreatment, by 52% and 72%, respectively. Dinoprostone 42-46 tumor necrosis factor Homo sapiens 63-72 10065947-3 1999 The cytokines IL-1beta and TNFalpha stimulated prostaglandin E2 (PGE2) and prostacyclin (PGI2) production in gingival fibroblasts. Dinoprostone 47-63 tumor necrosis factor Homo sapiens 27-35 10065947-3 1999 The cytokines IL-1beta and TNFalpha stimulated prostaglandin E2 (PGE2) and prostacyclin (PGI2) production in gingival fibroblasts. Dinoprostone 65-69 tumor necrosis factor Homo sapiens 27-35 10065947-4 1999 Simultaneous treatment of the cells with IL-1beta and TNFalpha resulted in a synergistic stimulation of PGE2 and PGI2 formation. Dinoprostone 104-108 tumor necrosis factor Homo sapiens 54-62 10065947-7 1999 Simultaneous addition of IL-1beta and TNFalpha synergistically enhanced COX-2 mRNA levels, accompanied by a corresponding stimulation of PGE2 synthesis. Dinoprostone 137-141 tumor necrosis factor Homo sapiens 38-46 10065947-9 1999 PMA, known to activate protein kinase C (PKC), enhanced the stimulatory effect of IL-1beta, TNFalpha, and the combination on COX-2 mRNA levels accompanied by a corresponding increase in PGE2 production. Dinoprostone 186-190 tumor necrosis factor Homo sapiens 92-100 9893042-7 1998 TNF-alpha increased prostaglandin E2 production by 20-fold in Ad5LacZ-infected HT-29 cells compared with uninfected cells and was significantly inhibited in Ad5IkappaB-infected cells in agreement with the COX-2 mRNA findings. Dinoprostone 20-36 tumor necrosis factor Homo sapiens 0-9 9877447-3 1998 The purpose of this study was to investigate the effect of tumor necrosis factor-alpha (TNF-alpha) on the levels of cyclooxygenase, prostaglandin E2 production (PGE2), and expression of the PGE2 receptor subtype EP1 in amnion WISH cell culture. Dinoprostone 132-148 tumor necrosis factor Homo sapiens 59-86 9877447-3 1998 The purpose of this study was to investigate the effect of tumor necrosis factor-alpha (TNF-alpha) on the levels of cyclooxygenase, prostaglandin E2 production (PGE2), and expression of the PGE2 receptor subtype EP1 in amnion WISH cell culture. Dinoprostone 132-148 tumor necrosis factor Homo sapiens 88-97 9877447-3 1998 The purpose of this study was to investigate the effect of tumor necrosis factor-alpha (TNF-alpha) on the levels of cyclooxygenase, prostaglandin E2 production (PGE2), and expression of the PGE2 receptor subtype EP1 in amnion WISH cell culture. Dinoprostone 161-165 tumor necrosis factor Homo sapiens 59-86 9877447-3 1998 The purpose of this study was to investigate the effect of tumor necrosis factor-alpha (TNF-alpha) on the levels of cyclooxygenase, prostaglandin E2 production (PGE2), and expression of the PGE2 receptor subtype EP1 in amnion WISH cell culture. Dinoprostone 161-165 tumor necrosis factor Homo sapiens 88-97 9877447-9 1998 The results suggest that TNF-alpha may play a role in infection-induced preterm labor by its pleiotropic ability to simultaneously stimulate COX-2 activity, PGE2 concentrations, and PGE2 EP1 receptor levels in human amnion. Dinoprostone 157-161 tumor necrosis factor Homo sapiens 25-34 9870074-4 1998 RESULTS: Both IL-10 and IL-4 inhibited IL-1 beta- and TNF-alpha-induced PGE2 production but had no significant effects on the production of PGE2 under basal conditions. Dinoprostone 72-76 tumor necrosis factor Homo sapiens 54-63 9811056-8 1998 The inhibition was prevented by PGE2, indicating that the synergistic effect of IL-1alpha and TNFalpha was PGE2-mediated. Dinoprostone 32-36 tumor necrosis factor Homo sapiens 94-102 9811056-8 1998 The inhibition was prevented by PGE2, indicating that the synergistic effect of IL-1alpha and TNFalpha was PGE2-mediated. Dinoprostone 107-111 tumor necrosis factor Homo sapiens 94-102 9811056-12 1998 CONCLUSION: These findings suggest that IL-1alpha and TNFalpha synergistically stimulate the production of IL-11 via their effects on PGE2 production in the rheumatoid joint, and that atypical PKC may be another target for down-regulation of IL-11, the bone resorption-associated cytokine. Dinoprostone 134-138 tumor necrosis factor Homo sapiens 54-62 9755052-5 1998 Treatment for 24 h with interleukin-1beta (IL-1beta; 10 ng/ml) or tumor necrosis factor-alpha (50 ng/ml), respectively, elicited maximal 25- and 6-fold inductions of PGE2 synthesis in CCD-18Co cultures and similar results in primary fibroblast cultures; maximal inductions with IL-1beta in colonic epithelial cell lines were from zero to fivefold. Dinoprostone 166-170 tumor necrosis factor Homo sapiens 66-93 9758210-6 1998 HPASMC treated with 200 U/ml of IL-1beta and 500 U/ml of TNF alpha produced more COX metabolites such as 6-keto-PGF1alpha, thromboxane B2, PGF2alpha and PGE2 than control cells. Dinoprostone 153-157 tumor necrosis factor Homo sapiens 57-66 9743339-4 1998 Here we show that PGE2, although it does not induce final DC maturation by itself, synergizes with IL-1beta and TNF-alpha, and allows their effectiveness at 100-fold lower concentrations. Dinoprostone 18-22 tumor necrosis factor Homo sapiens 112-121 9743553-0 1998 A carbocyclic nucleoside analogue is a TNF-alpha inhibitor with immunosuppressive action: role of prostaglandin E2 and protein kinase C and comparison with pentoxifylline. Dinoprostone 98-114 tumor necrosis factor Homo sapiens 39-48 9645689-10 1998 These results demonstrate unequivocally that IL 1alpha and TNFalpha enhance human osteoclast formation and suggest that they mediate their effects through PGE2. Dinoprostone 155-159 tumor necrosis factor Homo sapiens 59-67 9587398-2 1998 We first determined the effects of tumor necrosis factor-alpha (TNF-alpha) and IL-10 on monocyte prostaglandin E2 (PGE2) production. Dinoprostone 97-113 tumor necrosis factor Homo sapiens 35-62 9690866-4 1998 Incubation of T 67 astroglial cell line with IL-beta (10 ng ml(-1)) and TNF-alpha (500 u ml(-1)) produced a significant (P<0.05) increase of both nitrite (the breakdown product of NO), cyclic GMP and PGE2 levels in cell supernatants. Dinoprostone 203-207 tumor necrosis factor Homo sapiens 72-81 9839700-9 1998 Also, TNF-alpha and -beta produced a concentration-dependent stimulation of PGE2 formation in cultured human PDL cells. Dinoprostone 76-80 tumor necrosis factor Homo sapiens 6-25 9839700-11 1998 In addition, a synergistic effect on the PGE2 response to IL-1 alpha or -1 beta was demonstrated when added in combination with TNF-alpha. Dinoprostone 41-45 tumor necrosis factor Homo sapiens 128-137 9531313-3 1998 IL-1beta and TNF-alpha expression and synthesis were up-regulated by rhIL-17 in a dose (ED50 was 50 +/- 9 ng/ml)- and time-dependent fashion, with cytokine accumulation reaching a zenith after 9 h. Release of IL-6, PGE2, IL-10, IL-12, IL-1R antagonist, and stromelysin was also stimulated by rhIL-17. Dinoprostone 215-219 tumor necrosis factor Homo sapiens 13-22 9587398-2 1998 We first determined the effects of tumor necrosis factor-alpha (TNF-alpha) and IL-10 on monocyte prostaglandin E2 (PGE2) production. Dinoprostone 115-119 tumor necrosis factor Homo sapiens 35-62 9587398-4 1998 Both TNF-alpha and lipopolysaccharide (LPS) caused a remarkable increase in monocyte PGE2 production. Dinoprostone 85-89 tumor necrosis factor Homo sapiens 5-14 9587398-7 1998 Next, we determined the effect of PGE2 on TNF-alpha mRNA expression in monocytes. Dinoprostone 34-38 tumor necrosis factor Homo sapiens 42-51 9587398-14 1998 These results indicate that TNF-alpha and PGE2 are key molecules for the induction of IL-10 in monocytes, and that IL-10, in turn, plays a crucial role in terminating the inflammatory cascade via downregulation of production of proinflammatory molecules including TNF-alpha and PGE2. Dinoprostone 42-46 tumor necrosis factor Homo sapiens 264-273 9587398-14 1998 These results indicate that TNF-alpha and PGE2 are key molecules for the induction of IL-10 in monocytes, and that IL-10, in turn, plays a crucial role in terminating the inflammatory cascade via downregulation of production of proinflammatory molecules including TNF-alpha and PGE2. Dinoprostone 278-282 tumor necrosis factor Homo sapiens 28-37 9690866-14 1998 The present experiments demonstrated that the release of PGE2 by astroglial cells pretreated with IL-1beta and TNF-alpha is due to enhanced COX-2 activity via activation of the L-arginine-NO pathway, and this may be relevant to the understanding of the pathophysiological mechanisms underlying neuroimmune disorders. Dinoprostone 57-61 tumor necrosis factor Homo sapiens 111-120 9633531-9 1998 In summary, we demonstrate that the potentiation of PGE2 production by TGF-beta 1 in IL-1 beta and TNF-alpha-treated fibroblasts is the result of transcriptional stimulation of the Cox-2 gene by IL-1 beta and TNF-alpha and the stabilization of the resulting transcripts by TGF-beta 1. Dinoprostone 52-56 tumor necrosis factor Homo sapiens 99-108 9633531-9 1998 In summary, we demonstrate that the potentiation of PGE2 production by TGF-beta 1 in IL-1 beta and TNF-alpha-treated fibroblasts is the result of transcriptional stimulation of the Cox-2 gene by IL-1 beta and TNF-alpha and the stabilization of the resulting transcripts by TGF-beta 1. Dinoprostone 52-56 tumor necrosis factor Homo sapiens 209-218 9561806-7 1998 Bone marrow stromal cells release PGE2 and LTB4 in response to phorbol myristic acetate (PMA) (1 microM) and tumor necrosis factor alpha (TNF-alpha) (10 ng/ml). Dinoprostone 34-38 tumor necrosis factor Homo sapiens 109-136 9561806-7 1998 Bone marrow stromal cells release PGE2 and LTB4 in response to phorbol myristic acetate (PMA) (1 microM) and tumor necrosis factor alpha (TNF-alpha) (10 ng/ml). Dinoprostone 34-38 tumor necrosis factor Homo sapiens 138-147 9401927-5 1997 This result suggests that endogenous prostaglandin E2 (PGE2) partially inhibits IL-1 or TNF-alpha-induced IL-6 production and that the enhancement of IL-6 production by IL-1 or TNF-alpha may not be caused through endogenous PGE2-induced cAMP-dependent pathway. Dinoprostone 37-53 tumor necrosis factor Homo sapiens 88-97 9675546-4 1998 We investigated the effects of KE-298 on the production of matrix metalloproteinases and tissue inhibitor-1 of metalloproteinases and bone absorptive mediators including interleukin (IL)-6 and prostaglandin (PG) E2 in tumor necrosis factor (TNF)-alpha-stimulated rheumatoid arthritis synoviocytes. Dinoprostone 193-214 tumor necrosis factor Homo sapiens 218-251 9393919-9 1997 Both IL-1beta and TNFalpha stimulated IL-6 and PGE2 release from the osteoblast-like cells. Dinoprostone 47-51 tumor necrosis factor Homo sapiens 18-26 9631245-4 1998 In this article, we describe the results of studies designed to determine the extent to which IL-10 contributes to the suppression of TNF-alpha generation from LPS-stimulated human monocytes evoked by 8-bromo cyclic AMP (8-Br-cAMP), rolipram, salbutamol, and prostaglandin E2 (PGE2). Dinoprostone 259-275 tumor necrosis factor Homo sapiens 134-143 9631245-4 1998 In this article, we describe the results of studies designed to determine the extent to which IL-10 contributes to the suppression of TNF-alpha generation from LPS-stimulated human monocytes evoked by 8-bromo cyclic AMP (8-Br-cAMP), rolipram, salbutamol, and prostaglandin E2 (PGE2). Dinoprostone 277-281 tumor necrosis factor Homo sapiens 134-143 9631245-5 1998 LPS evoked a time- and concentration-dependent generation of TNF-alpha (t1/2 = 4.5 h; EC50 = 273 pg/mL), which was inhibited by exogenous human recombinant (h) IL-10 (IC50 = 124 pg/mL), and by rolipram (EC50 = 420 nM), 8-Br-cAMP (EC50 = 77 (microM), PGE2 (EC50 = 15 nM) and salbutamol (EC50 = 20 nM). Dinoprostone 250-254 tumor necrosis factor Homo sapiens 61-70 9457465-10 1998 TNF-alpha, IL-1 beta, IL-6, and IL-10 were each synergistic or additive with PGE2 in upregulating the promoter. Dinoprostone 77-81 tumor necrosis factor Homo sapiens 0-9 9464843-4 1997 PGE2 primes naive T cells in a dose-dependent fashion for production of high levels of IL-4, IL-10 and IL-13, and very low levels of IL-2, interferon (IFN)-gamma, tumor necrosis factor (TNF)-alpha, and TNF-beta. Dinoprostone 0-4 tumor necrosis factor Homo sapiens 163-196 9330943-7 1997 Moreover, reducing the shedding of TNF-sR, particularly the TNF-sR75, with a synthetic inhibitor decreased TNF-alpha induced PGE2 production. Dinoprostone 125-129 tumor necrosis factor Homo sapiens 107-116 9330943-8 1997 CONCLUSION: TNF-R55 is the major receptor isoform transducing PGE2 and COX-2 responses to TNF-alpha in OA synovial fibroblasts; soluble receptors could be involved in facilitating the binding of TNF-alpha to its receptor. Dinoprostone 62-66 tumor necrosis factor Homo sapiens 90-99 9401927-5 1997 This result suggests that endogenous prostaglandin E2 (PGE2) partially inhibits IL-1 or TNF-alpha-induced IL-6 production and that the enhancement of IL-6 production by IL-1 or TNF-alpha may not be caused through endogenous PGE2-induced cAMP-dependent pathway. Dinoprostone 55-59 tumor necrosis factor Homo sapiens 88-97 9401927-5 1997 This result suggests that endogenous prostaglandin E2 (PGE2) partially inhibits IL-1 or TNF-alpha-induced IL-6 production and that the enhancement of IL-6 production by IL-1 or TNF-alpha may not be caused through endogenous PGE2-induced cAMP-dependent pathway. Dinoprostone 55-59 tumor necrosis factor Homo sapiens 177-186 9401927-5 1997 This result suggests that endogenous prostaglandin E2 (PGE2) partially inhibits IL-1 or TNF-alpha-induced IL-6 production and that the enhancement of IL-6 production by IL-1 or TNF-alpha may not be caused through endogenous PGE2-induced cAMP-dependent pathway. Dinoprostone 224-228 tumor necrosis factor Homo sapiens 88-97 9401927-5 1997 This result suggests that endogenous prostaglandin E2 (PGE2) partially inhibits IL-1 or TNF-alpha-induced IL-6 production and that the enhancement of IL-6 production by IL-1 or TNF-alpha may not be caused through endogenous PGE2-induced cAMP-dependent pathway. Dinoprostone 224-228 tumor necrosis factor Homo sapiens 177-186 9401927-10 1997 Accordingly, in inflamed periodontal tissues, gingival fibroblasts and periodontal ligament fibroblasts stimulated with pro-inflammatory cytokines such as IL-1 or TNF-alpha, may produce IL-6, and this production can be differentially modulated by endogenous PGE2, IL-6sR, T cell-derived cytokines such as IFN-gamma or IL-4, and glucocorticoids. Dinoprostone 258-262 tumor necrosis factor Homo sapiens 163-172 9336233-7 1997 SP also enhanced the small inducing effect of tumor necrosis factor-alpha (TNF-alpha) on IL-6 and PGE2 secretion and that of transforming growth factor-beta on PGE2 secretion. Dinoprostone 98-102 tumor necrosis factor Homo sapiens 46-73 9298541-27 1997 or novel EP-receptors mediate the inhibitory effect of PGE2 on TNF alpha generation. Dinoprostone 55-59 tumor necrosis factor Homo sapiens 63-72 9336233-7 1997 SP also enhanced the small inducing effect of tumor necrosis factor-alpha (TNF-alpha) on IL-6 and PGE2 secretion and that of transforming growth factor-beta on PGE2 secretion. Dinoprostone 98-102 tumor necrosis factor Homo sapiens 75-84 9440135-6 1997 Treatment of WISH cells with TNF-alpha (0.1 ng/mL-100 ng/mL) caused a dose-dependent increase in COX-2 expression and the subsequent biosynthesis of PGE2 that persisted for at least 48 hrs. Dinoprostone 149-153 tumor necrosis factor Homo sapiens 29-38 9440135-8 1997 TNF-alpha-stimulated COX-2 expression and the subsequent formation of PGE2 were inhibited by dexamethasone (0.1 microM). Dinoprostone 70-74 tumor necrosis factor Homo sapiens 0-9 9440135-9 1997 In addition, indomethacin (1 microM) and the novel COX-2-selective inhibitor, NS-398 (IC50 approximately 1.1 x 10(-9) M), attenuated TNF-alpha-elicited PGE2 production. Dinoprostone 152-156 tumor necrosis factor Homo sapiens 133-142 9298541-6 1997 Exposure of human monocytes to LPS (3 ng ml-1, approximately EC84) resulted in a time-dependent elaboration to TNF alpha which was suppressed in cells pretreated with prostaglandin E1 (PGe1), PGE2 and cicaprost. Dinoprostone 192-196 tumor necrosis factor Homo sapiens 111-120 9168911-5 1997 In endothelium-denuded segments of pulmonary artery, the inflammatory agennts tumor necrosis factor alpha, interleukin-1 beta, interferon gamma, and lipopolysaccharide stimulated the release of PGE2 and 8-iso PGF2 alpha, which were attenuated in both cases by the cyclo-oxygenase inhibitor indomethacin. Dinoprostone 194-198 tumor necrosis factor Homo sapiens 78-105 9306218-4 1997 Significant correlations were evident only between PGE2 and TNF-alpha levels in the linear hip group and PGE2 and IL-1 beta levels in the knee group. Dinoprostone 51-55 tumor necrosis factor Homo sapiens 60-69 9271310-5 1997 In contrast, both PGE2 and IL-10 suppressed LPS-stimulated TNF-alpha production by AM and monocytes. Dinoprostone 18-22 tumor necrosis factor Homo sapiens 59-68 9290146-11 1997 To be certain that TNF-alpha stimulated PGE2 production was, indeed, a result of COX-2 induction, RIAs were carried out with the COX-2-selective inhibitor NS-398. Dinoprostone 40-44 tumor necrosis factor Homo sapiens 19-28 9290146-12 1997 Cells stimulated with the NS-398 after TNF-alpha exposure demonstrated suppression of TNF-alpha-stimulated PGE2 formation. Dinoprostone 107-111 tumor necrosis factor Homo sapiens 39-48 9290146-12 1997 Cells stimulated with the NS-398 after TNF-alpha exposure demonstrated suppression of TNF-alpha-stimulated PGE2 formation. Dinoprostone 107-111 tumor necrosis factor Homo sapiens 86-95 9154331-11 1997 Both populations of cells were equally susceptible towards inhibition of TNF release by cyclic AMP elevating agents such as dibutyryl cyclic AMP, prostaglandin E2 (PGE2) or forskolin, which all led to a complete abrogation of TNF production in a concentration-dependent manner and which were more efficient than the glucocorticoid dexamethasone. Dinoprostone 146-162 tumor necrosis factor Homo sapiens 73-76 9154331-11 1997 Both populations of cells were equally susceptible towards inhibition of TNF release by cyclic AMP elevating agents such as dibutyryl cyclic AMP, prostaglandin E2 (PGE2) or forskolin, which all led to a complete abrogation of TNF production in a concentration-dependent manner and which were more efficient than the glucocorticoid dexamethasone. Dinoprostone 164-168 tumor necrosis factor Homo sapiens 73-76 9154331-18 1997 Tolafentrine or motapizone in the presence of either PDE4 inhibitor, completely abrogated TNF formation in the presence of PGE2. Dinoprostone 123-127 tumor necrosis factor Homo sapiens 90-93 8977210-1 1997 Synthesis of TNF-alpha and IL-1beta, by monocytes/macrophages can be partially regulated by the eicosanoid, PGE2. Dinoprostone 108-112 tumor necrosis factor Homo sapiens 13-22 9093911-5 1997 Thus, TGF beta and TNF exerted a regulation of hOB cell PG biosynthesis that was principally directed towards an increased PGE2 biosynthesis, with lesser effects on the production of other PG metabolites. Dinoprostone 123-127 tumor necrosis factor Homo sapiens 19-22 9093911-8 1997 However, the increased production of PGE2 resulting from TNF stimulation was blocked by the addition of an interleukin-1 beta (IL-1 beta) neutralizing antibody, suggesting that TNF regulation of hOB cell PG synthesis was secondary to its capacity to increase hOB cell IL-1 beta production. Dinoprostone 37-41 tumor necrosis factor Homo sapiens 57-60 9093911-8 1997 However, the increased production of PGE2 resulting from TNF stimulation was blocked by the addition of an interleukin-1 beta (IL-1 beta) neutralizing antibody, suggesting that TNF regulation of hOB cell PG synthesis was secondary to its capacity to increase hOB cell IL-1 beta production. Dinoprostone 37-41 tumor necrosis factor Homo sapiens 177-180 9138698-17 1997 Incubation of the cells with the cytokine mixture (IL-1 beta, TNF alpha, IFN gamma each at 10 ng ml-1 for 24 h) caused the accumulation of PGE2 and 6-keto-PGF1 alpha. Dinoprostone 139-143 tumor necrosis factor Homo sapiens 62-71 9138698-19 1997 In experiments where COX-2 metabolized endogenous stores of arachidonic acid, treatment of HASM cells with IL-1 beta in combination with TNF alpha caused a similar release of PGE2 to that when the three cytokines were given in combination. Dinoprostone 175-179 tumor necrosis factor Homo sapiens 137-146 9089795-5 1997 The addition of PGE2 or iloprost greatly decreased the amount of TNF-alpha measured in the supernatants, although the rates of inhibition differed according to the kind of stimulation. Dinoprostone 16-20 tumor necrosis factor Homo sapiens 65-74 9021546-0 1997 Cyclosporin A upregulates prostaglandin E2 production in human gingival fibroblasts challenged with tumor necrosis factor alpha in vitro. Dinoprostone 26-42 tumor necrosis factor Homo sapiens 100-127 9021546-1 1997 The effect of cyclosporin A (CsA) on prostaglandin E2 (PGE2) production in human gingival fibroblasts challenged with tumor necrosis factor alpha (TNF-alpha) was studied. Dinoprostone 37-53 tumor necrosis factor Homo sapiens 147-156 9021546-1 1997 The effect of cyclosporin A (CsA) on prostaglandin E2 (PGE2) production in human gingival fibroblasts challenged with tumor necrosis factor alpha (TNF-alpha) was studied. Dinoprostone 55-59 tumor necrosis factor Homo sapiens 118-145 9021546-1 1997 The effect of cyclosporin A (CsA) on prostaglandin E2 (PGE2) production in human gingival fibroblasts challenged with tumor necrosis factor alpha (TNF-alpha) was studied. Dinoprostone 55-59 tumor necrosis factor Homo sapiens 147-156 9021546-2 1997 TNF-alpha (1-100 ng/ml) dose-dependently stimulated PGE2 formation in 24 h cultures. Dinoprostone 52-56 tumor necrosis factor Homo sapiens 0-9 9021546-3 1997 CsA (1-100 ng/ml) did not induce PGE2 formation itself but potentiated TNF-alpha induced PGE2 formation in gingival fibroblasts in a manner dependent on the concentrations of both CsA and TNF-alpha. Dinoprostone 89-93 tumor necrosis factor Homo sapiens 71-80 9021546-3 1997 CsA (1-100 ng/ml) did not induce PGE2 formation itself but potentiated TNF-alpha induced PGE2 formation in gingival fibroblasts in a manner dependent on the concentrations of both CsA and TNF-alpha. Dinoprostone 89-93 tumor necrosis factor Homo sapiens 188-197 9021546-7 1997 The results indicate that CsA and TNF-alpha act in concert on PGE2 formation in gingival fibroblasts, which may be of importance in the pathogenesis of gingival overgrowth induced by the drug. Dinoprostone 62-66 tumor necrosis factor Homo sapiens 34-43 9023325-1 1997 These studies examined the signal transduction mechanisms by which prostaglandin (PG) E2 production can occur in human amnionic WISH cells in response to the stimuli okadaic acid, interleukin (IL)-1beta, tumor necrosis factor (TNF)-alpha, phorbol-12-myristate-13-acetate (PMA) or combinations of PMA with IL-1beta or TNF-alpha. Dinoprostone 67-88 tumor necrosis factor Homo sapiens 204-237 9023325-1 1997 These studies examined the signal transduction mechanisms by which prostaglandin (PG) E2 production can occur in human amnionic WISH cells in response to the stimuli okadaic acid, interleukin (IL)-1beta, tumor necrosis factor (TNF)-alpha, phorbol-12-myristate-13-acetate (PMA) or combinations of PMA with IL-1beta or TNF-alpha. Dinoprostone 67-88 tumor necrosis factor Homo sapiens 317-326 8977210-9 1997 These novel observations implicate TXA2 as an important paracrine or autocrine facilitator of TNF-alpha and IL-1beta production in stimulated human monocytes and suggest that levels of TNF-alpha and IL-1beta synthesis are determined in part by the balance between TXA2 and PGE2 production in human monocytes. Dinoprostone 273-277 tumor necrosis factor Homo sapiens 185-194 8845037-7 1996 Lipopolysaccharide-induced TNF alpha production was significantly reduced in a similar fashion for both cord and adult monocytes at high (> or = 10(-7)M) PGE2 concentration. Dinoprostone 157-161 tumor necrosis factor Homo sapiens 27-36 9010678-3 1996 These naturally occurring inhibitors of TNF are shown to be 10 times less effective than the bivalent antagonist of TNF, recombinant soluble TNF receptor p55-human gamma 3 fusion protein (rsTNFR-p55h gamma 3), in controlling the release of prostaglandin E2 (PGE2) and collagenase by fibroblasts, as well as in controlling T cell proliferation. Dinoprostone 240-256 tumor necrosis factor Homo sapiens 40-43 9010678-3 1996 These naturally occurring inhibitors of TNF are shown to be 10 times less effective than the bivalent antagonist of TNF, recombinant soluble TNF receptor p55-human gamma 3 fusion protein (rsTNFR-p55h gamma 3), in controlling the release of prostaglandin E2 (PGE2) and collagenase by fibroblasts, as well as in controlling T cell proliferation. Dinoprostone 240-256 tumor necrosis factor Homo sapiens 116-119 9010678-3 1996 These naturally occurring inhibitors of TNF are shown to be 10 times less effective than the bivalent antagonist of TNF, recombinant soluble TNF receptor p55-human gamma 3 fusion protein (rsTNFR-p55h gamma 3), in controlling the release of prostaglandin E2 (PGE2) and collagenase by fibroblasts, as well as in controlling T cell proliferation. Dinoprostone 240-256 tumor necrosis factor Homo sapiens 116-119 9010678-3 1996 These naturally occurring inhibitors of TNF are shown to be 10 times less effective than the bivalent antagonist of TNF, recombinant soluble TNF receptor p55-human gamma 3 fusion protein (rsTNFR-p55h gamma 3), in controlling the release of prostaglandin E2 (PGE2) and collagenase by fibroblasts, as well as in controlling T cell proliferation. Dinoprostone 258-262 tumor necrosis factor Homo sapiens 40-43 9010678-3 1996 These naturally occurring inhibitors of TNF are shown to be 10 times less effective than the bivalent antagonist of TNF, recombinant soluble TNF receptor p55-human gamma 3 fusion protein (rsTNFR-p55h gamma 3), in controlling the release of prostaglandin E2 (PGE2) and collagenase by fibroblasts, as well as in controlling T cell proliferation. Dinoprostone 258-262 tumor necrosis factor Homo sapiens 116-119 9010678-3 1996 These naturally occurring inhibitors of TNF are shown to be 10 times less effective than the bivalent antagonist of TNF, recombinant soluble TNF receptor p55-human gamma 3 fusion protein (rsTNFR-p55h gamma 3), in controlling the release of prostaglandin E2 (PGE2) and collagenase by fibroblasts, as well as in controlling T cell proliferation. Dinoprostone 258-262 tumor necrosis factor Homo sapiens 116-119 8879179-4 1996 In this study we provide evidence that human lung fibroblasts, through the release of soluble factors such as prostaglandin E2 (PGE2), inhibit both TNF messenger ribonucleic acid (mRNA) accumulation and TNF-alpha protein release by lipopolysaccharide (LPS)-activated human peripheral blood monocytes (PBM). Dinoprostone 110-126 tumor necrosis factor Homo sapiens 148-151 8879179-4 1996 In this study we provide evidence that human lung fibroblasts, through the release of soluble factors such as prostaglandin E2 (PGE2), inhibit both TNF messenger ribonucleic acid (mRNA) accumulation and TNF-alpha protein release by lipopolysaccharide (LPS)-activated human peripheral blood monocytes (PBM). Dinoprostone 110-126 tumor necrosis factor Homo sapiens 203-212 8879179-4 1996 In this study we provide evidence that human lung fibroblasts, through the release of soluble factors such as prostaglandin E2 (PGE2), inhibit both TNF messenger ribonucleic acid (mRNA) accumulation and TNF-alpha protein release by lipopolysaccharide (LPS)-activated human peripheral blood monocytes (PBM). Dinoprostone 128-132 tumor necrosis factor Homo sapiens 148-151 8879179-4 1996 In this study we provide evidence that human lung fibroblasts, through the release of soluble factors such as prostaglandin E2 (PGE2), inhibit both TNF messenger ribonucleic acid (mRNA) accumulation and TNF-alpha protein release by lipopolysaccharide (LPS)-activated human peripheral blood monocytes (PBM). Dinoprostone 128-132 tumor necrosis factor Homo sapiens 203-212 8879179-10 1996 Considering that exogenous PGE2 can inhibit TNF-alpha production by PBM, and that fibroblasts are a good source of PGE2, we determined the content of PGE2 in the FCM used in our experiments. Dinoprostone 27-31 tumor necrosis factor Homo sapiens 44-53 8879179-11 1996 We found a good correlation (r = 0.949) between the amount of PGE2 produced by fibroblasts and the degree of TNF-alpha inhibition exerted. Dinoprostone 62-66 tumor necrosis factor Homo sapiens 109-118 8915021-3 1996 Triclosan also reduced the PGE2 formation induced by TNFalpha. Dinoprostone 27-31 tumor necrosis factor Homo sapiens 53-61 8891757-3 1996 In the human osteoblastic cell line MG-63, IL-1 alpha (10-1000 pg/ml), IL-1 beta (3-300 pg/ml) and TNF-alpha (1-30 ng/ml) stimulated prostaglandin E2 (PGE2) formation and inhibited 1,25(OH)2-vitamin D3-induced osteocalcin biosynthesis as well as basal production of type I collagen. Dinoprostone 133-149 tumor necrosis factor Homo sapiens 99-108 8843783-0 1996 TNF-alpha-induced inhibition of PC synthesis by human type II pneumocytes is sequentially mediated by PGE2 and NO. Dinoprostone 102-106 tumor necrosis factor Homo sapiens 0-9 8843783-8 1996 TNF-alpha induced an increase in PGE2 and guanosine 3",5"-cyclic monophosphate cell content and in the NO release to the medium. Dinoprostone 33-37 tumor necrosis factor Homo sapiens 0-9 8843783-10 1996 Our results suggest that NO generation, secondary to PGE2 production, is responsible for the TNF-alpha-induced inhibition of PC synthesis by human type II pneumocytes. Dinoprostone 53-57 tumor necrosis factor Homo sapiens 93-102 8891757-3 1996 In the human osteoblastic cell line MG-63, IL-1 alpha (10-1000 pg/ml), IL-1 beta (3-300 pg/ml) and TNF-alpha (1-30 ng/ml) stimulated prostaglandin E2 (PGE2) formation and inhibited 1,25(OH)2-vitamin D3-induced osteocalcin biosynthesis as well as basal production of type I collagen. Dinoprostone 151-155 tumor necrosis factor Homo sapiens 99-108 8891757-5 1996 Four non-steroidal antiinflammatory drugs, indomethacin, flurbiprofen, naproxen and meclofenamic acid, inhibited basal, IL-1 beta- and TNF-alpha-stimulated PGE2 formation in the MG-63 cells without affecting IL-1 beta- or TNF-alpha-induced inhibition of osteocalcin and type I collagen formation. Dinoprostone 156-160 tumor necrosis factor Homo sapiens 135-144 8891757-5 1996 Four non-steroidal antiinflammatory drugs, indomethacin, flurbiprofen, naproxen and meclofenamic acid, inhibited basal, IL-1 beta- and TNF-alpha-stimulated PGE2 formation in the MG-63 cells without affecting IL-1 beta- or TNF-alpha-induced inhibition of osteocalcin and type I collagen formation. Dinoprostone 156-160 tumor necrosis factor Homo sapiens 222-231 8891757-6 1996 In isolated, non-transformed, human osteoblast-like cells, IL-1 beta and TNF-alpha stimulated PGE2 formation and concomitantly inhibited 1,25(OH)2-vitamin D3-stimulated osteocalcin biosynthesis, without affecting type I collagen formation. Dinoprostone 94-98 tumor necrosis factor Homo sapiens 73-82 8925408-8 1996 Furthermore, adenylate cyclase activation with prostaglandin E2 or dibutyryl cyclic AMP, inhibited exocytosis in response to TNF alpha and FMLP, while having no effect on the release induced by vanadate or PMA. Dinoprostone 47-63 tumor necrosis factor Homo sapiens 125-134 8897887-0 1996 Tumor necrosis factor-alpha induces Cl- and K+ secretion in human distal colon driven by prostaglandin E2. Dinoprostone 89-105 tumor necrosis factor Homo sapiens 0-27 8897887-11 1996 Radioimmunoassay of prostaglandin E2 (PGE2) in the serosal bathing solution revealed an increase in PGE2 production/release after addition of TNF-alpha, which paralleled the Isc response. Dinoprostone 20-36 tumor necrosis factor Homo sapiens 142-151 8897887-11 1996 Radioimmunoassay of prostaglandin E2 (PGE2) in the serosal bathing solution revealed an increase in PGE2 production/release after addition of TNF-alpha, which paralleled the Isc response. Dinoprostone 38-42 tumor necrosis factor Homo sapiens 142-151 8660816-0 1996 Prostaglandin-E2 regulation of tumor necrosis factor receptor release in human monocytic THP-1 cells. Dinoprostone 0-16 tumor necrosis factor Homo sapiens 31-52 8660816-1 1996 Recent in vitro studies indicate that tumor necrosis factor (TNF) production in human monocytic THP-1 cells is suppressed by action of arachidonic acid metabolite prostaglandin-E2 (PGE2). Dinoprostone 163-179 tumor necrosis factor Homo sapiens 38-59 8660816-1 1996 Recent in vitro studies indicate that tumor necrosis factor (TNF) production in human monocytic THP-1 cells is suppressed by action of arachidonic acid metabolite prostaglandin-E2 (PGE2). Dinoprostone 163-179 tumor necrosis factor Homo sapiens 61-64 8660816-1 1996 Recent in vitro studies indicate that tumor necrosis factor (TNF) production in human monocytic THP-1 cells is suppressed by action of arachidonic acid metabolite prostaglandin-E2 (PGE2). Dinoprostone 181-185 tumor necrosis factor Homo sapiens 38-59 8660816-1 1996 Recent in vitro studies indicate that tumor necrosis factor (TNF) production in human monocytic THP-1 cells is suppressed by action of arachidonic acid metabolite prostaglandin-E2 (PGE2). Dinoprostone 181-185 tumor necrosis factor Homo sapiens 61-64 8660816-2 1996 PGE2 stimulation of human monocytic cell line THP-1 demonstrates that PGE2 not only regulates TNF activity at production levels, but does so through the release of two soluble TNF receptors (BP-55, BP-75) as well. Dinoprostone 0-4 tumor necrosis factor Homo sapiens 94-97 8660816-2 1996 PGE2 stimulation of human monocytic cell line THP-1 demonstrates that PGE2 not only regulates TNF activity at production levels, but does so through the release of two soluble TNF receptors (BP-55, BP-75) as well. Dinoprostone 0-4 tumor necrosis factor Homo sapiens 176-179 8660816-2 1996 PGE2 stimulation of human monocytic cell line THP-1 demonstrates that PGE2 not only regulates TNF activity at production levels, but does so through the release of two soluble TNF receptors (BP-55, BP-75) as well. Dinoprostone 70-74 tumor necrosis factor Homo sapiens 94-97 8660816-2 1996 PGE2 stimulation of human monocytic cell line THP-1 demonstrates that PGE2 not only regulates TNF activity at production levels, but does so through the release of two soluble TNF receptors (BP-55, BP-75) as well. Dinoprostone 70-74 tumor necrosis factor Homo sapiens 176-179 8660816-3 1996 PGE2 can thus exert a regulatory effect on TNF biologic activity by interfering with its ability to reach cell membrane receptors. Dinoprostone 0-4 tumor necrosis factor Homo sapiens 43-46 8660816-6 1996 PGE2-stimulated THP-1 cells showed soluble 55- and 75-kDa TNF receptor release levels which exceeded that of spontaneous release at both 2- and 6-hr activation periods. Dinoprostone 0-4 tumor necrosis factor Homo sapiens 58-61 8660816-7 1996 The numbers of both membrane TNF receptors were significantly upregulated as well in PGE2-activated cells, whereas the levels of 55- and 75-kDa TNF receptor mRNA levels remained unchanged. Dinoprostone 85-89 tumor necrosis factor Homo sapiens 29-32 8660816-8 1996 Thus, PGE2 induces TNF receptor release primarily at posttranscriptional levels. Dinoprostone 6-10 tumor necrosis factor Homo sapiens 19-22 8660816-11 1996 Internalization and cleavage by protease are therefore critical factors in PGE2-induced release of soluble TNF receptor shedding. Dinoprostone 75-79 tumor necrosis factor Homo sapiens 107-110 8720407-10 1996 The prostaglandin E2 production was dramatically enhanced by additional interleukin-1 alpha, but decreased by the addition of tumor necrosis factor-alpha. Dinoprostone 4-20 tumor necrosis factor Homo sapiens 126-153 8601624-9 1996 In contrast, neutrophils primed with TNF and challenged with PGE2, a product of AA metabolism via the cyclooxygenase pathway, showed a reduced chemiluminescence response. Dinoprostone 61-65 tumor necrosis factor Homo sapiens 37-40 8630267-16 1996 Because PGE2 is reported to inhibit the expression of IL-1 and TNF genes, we inhibited PGE2 synthesis with indomethacin during culture in room air; the result was an increase in the release of IL-1 and TNF. Dinoprostone 8-12 tumor necrosis factor Homo sapiens 63-66 8630267-16 1996 Because PGE2 is reported to inhibit the expression of IL-1 and TNF genes, we inhibited PGE2 synthesis with indomethacin during culture in room air; the result was an increase in the release of IL-1 and TNF. Dinoprostone 87-91 tumor necrosis factor Homo sapiens 63-66 8630267-17 1996 In additional studies, adding PGE2 inhibited TNF release from the hypoxia cells to values near those of room-air controls. Dinoprostone 30-34 tumor necrosis factor Homo sapiens 45-48 8777276-13 1996 gamma-IFN and TGF-beta did not enhance PGE2 formation, nor did these cytokines potentiate IL-beta or TNF-alpha-induced PGE2 production. Dinoprostone 119-123 tumor necrosis factor Homo sapiens 101-110 8653494-3 1996 The stimulatory effect of TNF alpha on IL-1 beta production was accompanied by enhanced PGE2 formation. Dinoprostone 88-92 tumor necrosis factor Homo sapiens 26-35 8653494-4 1996 When PHT and TNF alpha were added simultaneously, the drug potentiated the stimulatory effect of TNF alpha on both IL-1 beta production and PGE2 formation. Dinoprostone 140-144 tumor necrosis factor Homo sapiens 13-22 8653494-4 1996 When PHT and TNF alpha were added simultaneously, the drug potentiated the stimulatory effect of TNF alpha on both IL-1 beta production and PGE2 formation. Dinoprostone 140-144 tumor necrosis factor Homo sapiens 97-106 8647958-1 1996 Relationship to tumor necrosis factor-dependent release of arachidonic acid and prostaglandin E2 in human monocytes. Dinoprostone 80-96 tumor necrosis factor Homo sapiens 16-37 8647958-9 1996 Monoclonal antibodies to TNF-alpha and pentoxyphylline (inhibitor of TNF synthesis) inhibited both AA and PGE2 release. Dinoprostone 106-110 tumor necrosis factor Homo sapiens 25-34 8647958-9 1996 Monoclonal antibodies to TNF-alpha and pentoxyphylline (inhibitor of TNF synthesis) inhibited both AA and PGE2 release. Dinoprostone 106-110 tumor necrosis factor Homo sapiens 25-28 8647958-12 1996 These data suggest that TNF dependent release of AA and PGE2 contributes to CMV-induced immunosuppression. Dinoprostone 56-60 tumor necrosis factor Homo sapiens 24-27 8888354-3 1996 The highest concentration of TNF-alpha (10(-8)M) significantly increased the cyclooxygenase pathway, with prostaglandin E2 (PGE2) being a major product. Dinoprostone 106-122 tumor necrosis factor Homo sapiens 29-38 8888354-3 1996 The highest concentration of TNF-alpha (10(-8)M) significantly increased the cyclooxygenase pathway, with prostaglandin E2 (PGE2) being a major product. Dinoprostone 124-128 tumor necrosis factor Homo sapiens 29-38 8888354-7 1996 However, a combination of TNF-alpha (10(-8)M) and A23187 (10(-6)M) caused an inhibitory effect on each agent-induced PGE2 or 15-HETE production. Dinoprostone 117-121 tumor necrosis factor Homo sapiens 26-35 8630267-4 1996 Because PGE2 is reported to inhibit interleukin 1 (IL-1) and tumor necrosis factor (TNF), it is likely that hypoxia, through changes in PGE2, will alter IL-1 and TNF release from the human alveolar macrophage. Dinoprostone 8-12 tumor necrosis factor Homo sapiens 61-82 8630267-4 1996 Because PGE2 is reported to inhibit interleukin 1 (IL-1) and tumor necrosis factor (TNF), it is likely that hypoxia, through changes in PGE2, will alter IL-1 and TNF release from the human alveolar macrophage. Dinoprostone 8-12 tumor necrosis factor Homo sapiens 84-87 8630267-4 1996 Because PGE2 is reported to inhibit interleukin 1 (IL-1) and tumor necrosis factor (TNF), it is likely that hypoxia, through changes in PGE2, will alter IL-1 and TNF release from the human alveolar macrophage. Dinoprostone 8-12 tumor necrosis factor Homo sapiens 162-165 8630267-4 1996 Because PGE2 is reported to inhibit interleukin 1 (IL-1) and tumor necrosis factor (TNF), it is likely that hypoxia, through changes in PGE2, will alter IL-1 and TNF release from the human alveolar macrophage. Dinoprostone 136-140 tumor necrosis factor Homo sapiens 61-82 8630267-4 1996 Because PGE2 is reported to inhibit interleukin 1 (IL-1) and tumor necrosis factor (TNF), it is likely that hypoxia, through changes in PGE2, will alter IL-1 and TNF release from the human alveolar macrophage. Dinoprostone 136-140 tumor necrosis factor Homo sapiens 84-87 8630267-4 1996 Because PGE2 is reported to inhibit interleukin 1 (IL-1) and tumor necrosis factor (TNF), it is likely that hypoxia, through changes in PGE2, will alter IL-1 and TNF release from the human alveolar macrophage. Dinoprostone 136-140 tumor necrosis factor Homo sapiens 162-165 8777276-2 1996 IL-1 alpha, IL-1 beta, TNF-alpha and TNF-beta caused a time- and concentration-dependent enhancement of prostaglandin E2 (PGE2) formation in the fibroblasts. Dinoprostone 104-120 tumor necrosis factor Homo sapiens 23-32 8777276-2 1996 IL-1 alpha, IL-1 beta, TNF-alpha and TNF-beta caused a time- and concentration-dependent enhancement of prostaglandin E2 (PGE2) formation in the fibroblasts. Dinoprostone 122-126 tumor necrosis factor Homo sapiens 23-32 8777276-6 1996 BK and thrombin also synergistically potentiated the stimulatory effect of TNF-alpha and TNF-beta on PGE2 formation. Dinoprostone 101-105 tumor necrosis factor Homo sapiens 75-84 8777276-8 1996 BK analogues with affinity to BK B2-receptors, but not to BK B1-receptors, were able to synergistically potentiate IL-1 beta and TNF-alpha-enhanced PGE2 production. Dinoprostone 148-152 tumor necrosis factor Homo sapiens 129-138 8777276-9 1996 The synergistic stimulation of PGE2 formation by IL-1, TNF and BK was abolished by indomethacin and flurbiprofen. Dinoprostone 31-35 tumor necrosis factor Homo sapiens 55-58 8777276-10 1996 Preincubation with IL-1 beta and TNF-alpha for 24 h resulted in a substantial amplification of the PGE2 response to a subsequent 24 h challenge with BK in the absence of cytokine. Dinoprostone 99-103 tumor necrosis factor Homo sapiens 33-42 8777276-11 1996 Similarly, when the pulp fibroblasts were preincubated with or without IL-1 beta or TNF-alpha for 24 h and then challenged with exogenous arachidonic acid for 60 min, PGE2 formation was significantly enhanced in cytokine pretreated cells. Dinoprostone 167-171 tumor necrosis factor Homo sapiens 84-93 8821840-3 1996 Spontaneous release of tumour necrosis factor alpha (TNF alpha) and interleukins 6 (IL-6) by PM luminal diameter of, after 4 or 24 hours in culture, increased significantly with time on CAPD, while there was a small but significant decrease in release of prostaglandin E2 (PGE2). Dinoprostone 255-271 tumor necrosis factor Homo sapiens 53-62 8821840-3 1996 Spontaneous release of tumour necrosis factor alpha (TNF alpha) and interleukins 6 (IL-6) by PM luminal diameter of, after 4 or 24 hours in culture, increased significantly with time on CAPD, while there was a small but significant decrease in release of prostaglandin E2 (PGE2). Dinoprostone 273-277 tumor necrosis factor Homo sapiens 53-62 8589268-9 1995 Culture with PGE2 alone suppressed TNF production by three of the six TCC and NK cell lines, which was neutralized by addition of IM. Dinoprostone 13-17 tumor necrosis factor Homo sapiens 35-38 8555055-2 1995 The TNF-triggered O2- production was significantly reduced by 10 microM prostaglandin E2 (PGE2), which was ineffective at lower doses. Dinoprostone 72-88 tumor necrosis factor Homo sapiens 4-7 8555055-2 1995 The TNF-triggered O2- production was significantly reduced by 10 microM prostaglandin E2 (PGE2), which was ineffective at lower doses. Dinoprostone 90-94 tumor necrosis factor Homo sapiens 4-7 8555055-4 1995 When PGE2 and RO 20-1724 were added together to TNF-triggered neutrophils they caused a marked synergistic inhibition of O2- production. Dinoprostone 5-9 tumor necrosis factor Homo sapiens 48-51 8555055-6 1995 These results suggest that cyclic AMP (cAMP)-elevating agents (PGE2, FK, RO 20-1724) down-regulate the capacity of adherent neutrophils to mount the respiratory burst in response to TNF. Dinoprostone 63-67 tumor necrosis factor Homo sapiens 182-185 8555055-10 1995 In conclusion, taking into account the TNF capacity to promote PGE2 formation at sites of inflammation, our observations suggest the existence of a negative PGE2-dependent feed-back, potentially capable of controlling the neutrophil response to TNF and susceptible to amplification by PDE IV-inhibiting compounds. Dinoprostone 63-67 tumor necrosis factor Homo sapiens 39-42 8555055-10 1995 In conclusion, taking into account the TNF capacity to promote PGE2 formation at sites of inflammation, our observations suggest the existence of a negative PGE2-dependent feed-back, potentially capable of controlling the neutrophil response to TNF and susceptible to amplification by PDE IV-inhibiting compounds. Dinoprostone 63-67 tumor necrosis factor Homo sapiens 245-248 8555055-10 1995 In conclusion, taking into account the TNF capacity to promote PGE2 formation at sites of inflammation, our observations suggest the existence of a negative PGE2-dependent feed-back, potentially capable of controlling the neutrophil response to TNF and susceptible to amplification by PDE IV-inhibiting compounds. Dinoprostone 157-161 tumor necrosis factor Homo sapiens 39-42 8555055-10 1995 In conclusion, taking into account the TNF capacity to promote PGE2 formation at sites of inflammation, our observations suggest the existence of a negative PGE2-dependent feed-back, potentially capable of controlling the neutrophil response to TNF and susceptible to amplification by PDE IV-inhibiting compounds. Dinoprostone 157-161 tumor necrosis factor Homo sapiens 245-248 8673868-10 1995 TNF stimulates surrounding osteoblasts to produce GM-CSF, IL-6, and PGE-2 which leads to recruitment of macrophages and osteoclasts into the area of the bone-cement interface. Dinoprostone 68-73 tumor necrosis factor Homo sapiens 0-3 7544757-11 1995 Thus, we conclude that AFP downregulates TNF-alpha and IL-1 beta production via a PGE2-dependent mechanism. Dinoprostone 82-86 tumor necrosis factor Homo sapiens 41-50 8785034-5 1996 Exogenous and endogenous prostaglandin E2 (PGE2) was found to inhibit the release of TNF alpha rather than IL-1 beta from peritoneal macrophages, indicating that the synthesis and secretion of these cytokines is distinctly regulated by PGE2. Dinoprostone 25-41 tumor necrosis factor Homo sapiens 85-94 8785034-5 1996 Exogenous and endogenous prostaglandin E2 (PGE2) was found to inhibit the release of TNF alpha rather than IL-1 beta from peritoneal macrophages, indicating that the synthesis and secretion of these cytokines is distinctly regulated by PGE2. Dinoprostone 43-47 tumor necrosis factor Homo sapiens 85-94 8785034-5 1996 Exogenous and endogenous prostaglandin E2 (PGE2) was found to inhibit the release of TNF alpha rather than IL-1 beta from peritoneal macrophages, indicating that the synthesis and secretion of these cytokines is distinctly regulated by PGE2. Dinoprostone 236-240 tumor necrosis factor Homo sapiens 85-94 8805102-5 1996 Prostaglandin E2 depressed the production of IL-1 alpha, while it up-regulated the production of IL-6, TNF-alpha, and IFN-gamma. Dinoprostone 0-16 tumor necrosis factor Homo sapiens 103-112 8554585-6 1995 TNF alpha activated PLA2 in hepatocytes and it is believed that the subsequent production of PGE2 plays a role in the "priming" process in these cells and at the same time amplifies the proliferating signals induced by hepatocyte-specific growth factors. Dinoprostone 93-97 tumor necrosis factor Homo sapiens 0-9 7492275-0 1995 Both prostaglandin E2 and nitric oxide sequentially mediate the tumor necrosis factor alpha-induced inhibition of surfactant synthesis by human type II pneumocytes. Dinoprostone 5-21 tumor necrosis factor Homo sapiens 64-91 7492275-10 1995 Tumor necrosis factor alpha induced an increase in PGE2 (4.31 +/- 0.27 vs 1.65 +/- 0.17-pg/microgram protein, n = 10, P < .01) and cGMP (0.238 +/- 0.012 vs 0.109 +/- 0.014-pmol/microgram protein, n = 10, P < .01) cell content and in the NO release to the medium (3.10 +/- 0.14 vs 1.19 +/- 0.11-nmol/microgram protein, n = 10, P < .01). Dinoprostone 51-55 tumor necrosis factor Homo sapiens 0-27 7492275-14 1995 CONCLUSIONS: The NO generation, secondary to PGE2 production, seems responsible for the TNF-alpha-induced inhibition of phosphatidylcholine synthesis by human type II pneumocytes. Dinoprostone 45-49 tumor necrosis factor Homo sapiens 88-97 8705835-5 1995 Tumour necrosis factor alpha (TNF alpha) and interleukin-I (IL-I) are markedly proinflammatory, inducing bone resorption, collagenase and prostaglandin E2 production. Dinoprostone 138-154 tumor necrosis factor Homo sapiens 30-39 8545605-1 1995 BACKGROUND: We have recently reported that tumor necrosis factor-alpha (TNF-alpha), a pro-inflammatory cytokine that has been suggested to play a role in the pathogenesis of inflammatory bowel disease, potentiates phospholipase A2 (PLA2)-stimulated arachidonic acid (AA) release and prostaglandin E2 (PGE2) formation in cultured intestinal epithelial cells (INT 407). Dinoprostone 283-299 tumor necrosis factor Homo sapiens 43-70 8545605-1 1995 BACKGROUND: We have recently reported that tumor necrosis factor-alpha (TNF-alpha), a pro-inflammatory cytokine that has been suggested to play a role in the pathogenesis of inflammatory bowel disease, potentiates phospholipase A2 (PLA2)-stimulated arachidonic acid (AA) release and prostaglandin E2 (PGE2) formation in cultured intestinal epithelial cells (INT 407). Dinoprostone 283-299 tumor necrosis factor Homo sapiens 72-81 8545605-1 1995 BACKGROUND: We have recently reported that tumor necrosis factor-alpha (TNF-alpha), a pro-inflammatory cytokine that has been suggested to play a role in the pathogenesis of inflammatory bowel disease, potentiates phospholipase A2 (PLA2)-stimulated arachidonic acid (AA) release and prostaglandin E2 (PGE2) formation in cultured intestinal epithelial cells (INT 407). Dinoprostone 301-305 tumor necrosis factor Homo sapiens 43-70 8545605-1 1995 BACKGROUND: We have recently reported that tumor necrosis factor-alpha (TNF-alpha), a pro-inflammatory cytokine that has been suggested to play a role in the pathogenesis of inflammatory bowel disease, potentiates phospholipase A2 (PLA2)-stimulated arachidonic acid (AA) release and prostaglandin E2 (PGE2) formation in cultured intestinal epithelial cells (INT 407). Dinoprostone 301-305 tumor necrosis factor Homo sapiens 72-81 8545605-7 1995 The TNF-alpha-potentiated PGE2 release was reduced after inhibition of cellular COX activity or mRNA synthesis. Dinoprostone 26-30 tumor necrosis factor Homo sapiens 4-13 7747431-0 1995 HIV-induced TNF-alpha regulates arachidonic acid and PGE2 release from HIV-infected mononuclear phagocytes. Dinoprostone 53-57 tumor necrosis factor Homo sapiens 12-21 7747431-14 1995 Treating monocyte and macrophage cultures with mAb to TNF-alpha inhibited the HIV-induced release of AA and PGE2. Dinoprostone 108-112 tumor necrosis factor Homo sapiens 54-63 7547677-7 1995 Paradoxically, drugs that effectively inhibit expression of TNF-alpha via the elevation of intracellular cAMP level (iloprost, pentoxifylline, prostaglandin E2 and N6,2-O-dibutyryl cAMP) augmented the endotoxin-induced IL-10 synthesis at both protein and mRNA levels. Dinoprostone 143-159 tumor necrosis factor Homo sapiens 60-69 7747431-15 1995 These findings indicate that HIV-induced TNF-alpha regulates the release of AA and PGE2, which might provide insight into the mechanisms involved in the pathogenesis of HIV-related disorders. Dinoprostone 83-87 tumor necrosis factor Homo sapiens 41-50 7774879-8 1995 Furthermore the TNF stimulation increased glial fibrillary acidic protein and production of bioactive molecules including interleukin(IL)-6, IL-8, granulocyte-macrophage colony stimulating factor, prostaglandin E2 and manganous superoxide dismutase. Dinoprostone 197-213 tumor necrosis factor Homo sapiens 16-19 7717321-5 1995 The PGE2 values correlated well with the released concentrations of eosinophil cationic protein, myeloperoxidase, and tumor necrosis factor-alpha. Dinoprostone 4-8 tumor necrosis factor Homo sapiens 68-145 7751029-4 1995 We demonstrated that PGE2, CT and 8-bromo-cAMP inhibited the LPS-induced gene activation of TNF-alpha and IL-1 alpha, and had no effect on the gene activation of IL-1 beta and IL-8. Dinoprostone 21-25 tumor necrosis factor Homo sapiens 92-101 7532667-5 1995 In addition, treatment with either isoproterenol or prostaglandin E2, which activates receptors coupled to Gs and increases [cAMP]i, also inhibited TNF-alpha-induced expression of ICAM-1 and VCAM-1 on ASM. Dinoprostone 52-68 tumor necrosis factor Homo sapiens 148-157 7532667-6 1995 Furthermore, adhesion of activated T cells to TNF-alpha-stimulated ASM was inhibited by treating the ASM cells with either forskolin or PGE2. Dinoprostone 136-140 tumor necrosis factor Homo sapiens 46-55 7734430-10 1995 The correlation between TNF-alpha and PGE2 levels was .5 between IL-6 and PGE2 was .6, and between IL-6 and TNF-alpha was .77. Dinoprostone 38-42 tumor necrosis factor Homo sapiens 24-33 7734430-10 1995 The correlation between TNF-alpha and PGE2 levels was .5 between IL-6 and PGE2 was .6, and between IL-6 and TNF-alpha was .77. Dinoprostone 74-78 tumor necrosis factor Homo sapiens 24-33 7877083-0 1994 Prostaglandin E2 inhibits interleukin-6 release but not its transcription in human gingival fibroblasts stimulated with interleukin-1 beta or tumor necrosis factor-alpha. Dinoprostone 0-16 tumor necrosis factor Homo sapiens 142-169 7699295-7 1995 The production of prostaglandin E2 in vitro was dramatically increased by the addition of IL-1 alpha and decreased by the addition of TNF-alpha. Dinoprostone 18-34 tumor necrosis factor Homo sapiens 134-143 7877083-2 1994 The purpose of this study was to examine whether prostaglandin E2 (PGE2), which is produced in abundance from HGF after stimulation with interleukin (IL)-1 beta or tumor necrosis factor-alpha (TNF-alpha), could regulate IL-6 production by HGF. Dinoprostone 49-65 tumor necrosis factor Homo sapiens 164-191 7877083-2 1994 The purpose of this study was to examine whether prostaglandin E2 (PGE2), which is produced in abundance from HGF after stimulation with interleukin (IL)-1 beta or tumor necrosis factor-alpha (TNF-alpha), could regulate IL-6 production by HGF. Dinoprostone 49-65 tumor necrosis factor Homo sapiens 193-202 7877083-2 1994 The purpose of this study was to examine whether prostaglandin E2 (PGE2), which is produced in abundance from HGF after stimulation with interleukin (IL)-1 beta or tumor necrosis factor-alpha (TNF-alpha), could regulate IL-6 production by HGF. Dinoprostone 67-71 tumor necrosis factor Homo sapiens 164-191 7877083-2 1994 The purpose of this study was to examine whether prostaglandin E2 (PGE2), which is produced in abundance from HGF after stimulation with interleukin (IL)-1 beta or tumor necrosis factor-alpha (TNF-alpha), could regulate IL-6 production by HGF. Dinoprostone 67-71 tumor necrosis factor Homo sapiens 193-202 7877083-4 1994 IL-6 secretion from either IL-1 beta- or TNF-alpha-stimulated HGF was enhanced by the inhibition of PGE2 synthesis with indomethacin. Dinoprostone 100-104 tumor necrosis factor Homo sapiens 41-50 8080195-0 1994 Normal M phi cell-associated TNF alpha is resistant to PGE2 as well as TGF beta downregulation. Dinoprostone 55-59 tumor necrosis factor Homo sapiens 29-38 7892510-11 1994 The PGE2-stimulatory activity present in the other peak contained IL-1 beta, epidermal growth factor (EGF), and tumor necrosis factor-alpha (TNF-alpha). Dinoprostone 4-8 tumor necrosis factor Homo sapiens 112-139 7892510-11 1994 The PGE2-stimulatory activity present in the other peak contained IL-1 beta, epidermal growth factor (EGF), and tumor necrosis factor-alpha (TNF-alpha). Dinoprostone 4-8 tumor necrosis factor Homo sapiens 141-150 7892510-13 1994 We have previously shown that TGF-alpha and EGF are synergistic with IL-1 and TNF-alpha in enhancing amnion cell PGE2 production. Dinoprostone 113-117 tumor necrosis factor Homo sapiens 78-87 8014195-7 1994 Although the effects of PGE2 did not potentiate those of IL-1 on collagenase gene expression in vitro, one could speculate that massive production of PGE2 by connective tissue cells in vivo in response to inflammatory mediators such as IL-1 or tumor necrosis factor-alpha, could lead to sustained expression of collagenase in connective tissue cells after clearance of the growth factors. Dinoprostone 150-154 tumor necrosis factor Homo sapiens 244-271 8002047-6 1994 Increasing PGE2 down regulated the TNF-alpha production, but did not effect the IL-1 beta and IL-6 production. Dinoprostone 11-15 tumor necrosis factor Homo sapiens 35-44 8295980-1 1993 The purpose of this study was to determine how tumor necrosis factor alpha (TNF alpha) stimulates prostaglandin E2 production in human amnion. Dinoprostone 98-114 tumor necrosis factor Homo sapiens 47-74 9419743-5 1994 RESULTS: The concentration-related stimulation of decidual PGE2 production by IL-1 beta and TNF alpha was completely abrogated by cycloheximide and actinomycin D treatment. Dinoprostone 59-63 tumor necrosis factor Homo sapiens 92-101 8267584-4 1993 IL-4 (10 ng/ml) alone did not affect prostaglandin E2 (PGE2) synthesis by mesangial cells, though, it inhibited IL-1 alpha- and TNF alpha-stimulated PGE2 synthesis by 48% and 81%, respectively. Dinoprostone 149-153 tumor necrosis factor Homo sapiens 128-137 8140119-1 1993 Interleukin-1 (IL-1), tumor necrosis factor (TNF), epidermal growth factor (EGF), and transforming growth factor-alpha (TGF-alpha) stimulate prostaglandin E2 (PGE2) production by amnion cells whereas TGF-beta inhibits the PGE2 production. Dinoprostone 159-163 tumor necrosis factor Homo sapiens 86-118 8140119-1 1993 Interleukin-1 (IL-1), tumor necrosis factor (TNF), epidermal growth factor (EGF), and transforming growth factor-alpha (TGF-alpha) stimulate prostaglandin E2 (PGE2) production by amnion cells whereas TGF-beta inhibits the PGE2 production. Dinoprostone 222-226 tumor necrosis factor Homo sapiens 22-43 8140119-1 1993 Interleukin-1 (IL-1), tumor necrosis factor (TNF), epidermal growth factor (EGF), and transforming growth factor-alpha (TGF-alpha) stimulate prostaglandin E2 (PGE2) production by amnion cells whereas TGF-beta inhibits the PGE2 production. Dinoprostone 222-226 tumor necrosis factor Homo sapiens 86-118 8140119-6 1993 IL-1 or TNF in combination with EGF or TGF-alpha stimulated synergistically the production of PGE2 by amnion cells. Dinoprostone 94-98 tumor necrosis factor Homo sapiens 8-11 8140119-0 1993 Epidermal growth factor and transforming growth factor-alpha enhance the interleukin-1- and tumor necrosis factor-stimulated prostaglandin E2 production and the interleukin-1 specific binding on amnion cells. Dinoprostone 125-141 tumor necrosis factor Homo sapiens 28-60 8140119-1 1993 Interleukin-1 (IL-1), tumor necrosis factor (TNF), epidermal growth factor (EGF), and transforming growth factor-alpha (TGF-alpha) stimulate prostaglandin E2 (PGE2) production by amnion cells whereas TGF-beta inhibits the PGE2 production. Dinoprostone 141-157 tumor necrosis factor Homo sapiens 22-43 8140119-1 1993 Interleukin-1 (IL-1), tumor necrosis factor (TNF), epidermal growth factor (EGF), and transforming growth factor-alpha (TGF-alpha) stimulate prostaglandin E2 (PGE2) production by amnion cells whereas TGF-beta inhibits the PGE2 production. Dinoprostone 141-157 tumor necrosis factor Homo sapiens 45-48 8140119-1 1993 Interleukin-1 (IL-1), tumor necrosis factor (TNF), epidermal growth factor (EGF), and transforming growth factor-alpha (TGF-alpha) stimulate prostaglandin E2 (PGE2) production by amnion cells whereas TGF-beta inhibits the PGE2 production. Dinoprostone 141-157 tumor necrosis factor Homo sapiens 86-118 8140119-1 1993 Interleukin-1 (IL-1), tumor necrosis factor (TNF), epidermal growth factor (EGF), and transforming growth factor-alpha (TGF-alpha) stimulate prostaglandin E2 (PGE2) production by amnion cells whereas TGF-beta inhibits the PGE2 production. Dinoprostone 159-163 tumor necrosis factor Homo sapiens 22-43 8140119-1 1993 Interleukin-1 (IL-1), tumor necrosis factor (TNF), epidermal growth factor (EGF), and transforming growth factor-alpha (TGF-alpha) stimulate prostaglandin E2 (PGE2) production by amnion cells whereas TGF-beta inhibits the PGE2 production. Dinoprostone 159-163 tumor necrosis factor Homo sapiens 45-48 8295980-1 1993 The purpose of this study was to determine how tumor necrosis factor alpha (TNF alpha) stimulates prostaglandin E2 production in human amnion. Dinoprostone 98-114 tumor necrosis factor Homo sapiens 76-85 8295980-5 1993 The stimulatory action of TNF alpha on amnion PGE2 production was blocked by protein synthesis inhibitors, and the addition of arachidonic acid always enhanced the stimulatory properties of TNF alpha. Dinoprostone 46-50 tumor necrosis factor Homo sapiens 26-35 8295980-7 1993 These results suggest that the stimulatory action of TNF alpha on amnion PGE2 production is likely at the level of induction of fatty acid cyclooxygenase activity and is partially dependent upon activation of protein kinase C. Dinoprostone 73-77 tumor necrosis factor Homo sapiens 53-62 7507098-6 1993 Moreover, the prostacyclin analogs as well as PGE2 suppressed LPS-induced production of TNF-alpha in Mono Mac 6 cells, a permanent human cell line with characteristics of mature monocytes. Dinoprostone 46-50 tumor necrosis factor Homo sapiens 88-97 7507098-1 1993 Recent reports have shown that prostaglandin E2 (PGE2) is able to suppress lipopolysaccharide (LPS)-stimulated production of tumor necrosis factor-alpha (TNF-alpha). Dinoprostone 31-47 tumor necrosis factor Homo sapiens 125-152 7507098-1 1993 Recent reports have shown that prostaglandin E2 (PGE2) is able to suppress lipopolysaccharide (LPS)-stimulated production of tumor necrosis factor-alpha (TNF-alpha). Dinoprostone 31-47 tumor necrosis factor Homo sapiens 154-163 7507098-7 1993 Suppression of TNF-alpha synthesis by cicaprost and PGE2 is probably mediated by an increased intracellular cAMP formation. Dinoprostone 52-56 tumor necrosis factor Homo sapiens 15-24 7507098-1 1993 Recent reports have shown that prostaglandin E2 (PGE2) is able to suppress lipopolysaccharide (LPS)-stimulated production of tumor necrosis factor-alpha (TNF-alpha). Dinoprostone 49-53 tumor necrosis factor Homo sapiens 125-152 7507098-1 1993 Recent reports have shown that prostaglandin E2 (PGE2) is able to suppress lipopolysaccharide (LPS)-stimulated production of tumor necrosis factor-alpha (TNF-alpha). Dinoprostone 49-53 tumor necrosis factor Homo sapiens 154-163 8311923-2 1993 METHODS: IL-1 beta, TNF alpha, and EGF induced a concentration-related stimulation of prostaglandin E2 (PGE2) biosynthesis in human chorion cells, and this stimulation was enhanced by the addition of exogenous arachidonic acid. Dinoprostone 86-102 tumor necrosis factor Homo sapiens 20-29 7507098-2 1993 In the present study we compared PGE2 with prostacyclin (PGI2) analogs in their potency to influence LPS-stimulated production of interleukin-1 beta (IL-1 beta) and TNF-alpha by human mononuclear cells (MNC). Dinoprostone 33-37 tumor necrosis factor Homo sapiens 165-174 8409518-3 1993 The present study deals with the autocrine roles of UVB-induced, keratinocyte-derived cytokines IL-1 and tumor-necrosis-factor (TNF) alpha and their corresponding receptor molecules for UVB-induced PGE2 release. Dinoprostone 198-202 tumor necrosis factor Homo sapiens 105-138 8409518-7 1993 Addition of recombinant human TNF alpha to unirradiated KB cells resulted in five- to eightfold increased PGE2 synthesis, and this increase could be mimicked by stimulation of KB cells with MoAb htr-9, which exerts TNF alpha-like bioactivity by binding to the 55-kD TNF receptor (TNFR). Dinoprostone 106-110 tumor necrosis factor Homo sapiens 30-39 8409518-8 1993 UVB-induced PGE2 synthesis was blocked by 50% in the presence of neutralizing anti-TNF alpha-Ab, and was completely inhibited by addition of both anti-TNF alpha-Ab and MoAb M4. Dinoprostone 12-16 tumor necrosis factor Homo sapiens 83-86 8409518-8 1993 UVB-induced PGE2 synthesis was blocked by 50% in the presence of neutralizing anti-TNF alpha-Ab, and was completely inhibited by addition of both anti-TNF alpha-Ab and MoAb M4. Dinoprostone 12-16 tumor necrosis factor Homo sapiens 83-92 8409518-11 1993 These studies indicate that keratinocyte-derived TNF alpha and IL-1 together mediate UVB-induced PGE2 release via specific cell surface receptors, and that one intracellular mechanism is an increased prostanoid-synthesizing capacity of irradiated cells. Dinoprostone 97-101 tumor necrosis factor Homo sapiens 49-58 8248548-4 1993 Addition of TNF-alpha to the fetal side of the membrane increased production of PGE2 by amnion and PGE2 metabolites from chorion. Dinoprostone 80-84 tumor necrosis factor Homo sapiens 12-21 8248548-4 1993 Addition of TNF-alpha to the fetal side of the membrane increased production of PGE2 by amnion and PGE2 metabolites from chorion. Dinoprostone 99-103 tumor necrosis factor Homo sapiens 12-21 8311923-2 1993 METHODS: IL-1 beta, TNF alpha, and EGF induced a concentration-related stimulation of prostaglandin E2 (PGE2) biosynthesis in human chorion cells, and this stimulation was enhanced by the addition of exogenous arachidonic acid. Dinoprostone 104-108 tumor necrosis factor Homo sapiens 20-29 8311923-3 1993 RESULTS: Protein synthesis inhibition with cycloheximide or actinomycin D resulted in complete abrogation of the stimulation of PGE2 production by IL-1 beta, TNF alpha, and EGF. Dinoprostone 128-132 tumor necrosis factor Homo sapiens 158-167 8311923-5 1993 CONCLUSIONS: It is suggested that IL-1 beta, TNF alpha, and EGF all act to stimulate human chorion PGE2 production primarily via induction of prostaglandin endoperoxide synthase activity. Dinoprostone 99-103 tumor necrosis factor Homo sapiens 45-54 8244447-4 1993 Because M phi produce tumor necrosis factor-alpha (TNF-alpha) during cancer, and TNF-alpha stimulates M phi PGE2 synthesis, we determined if TNF-alpha mediates tumor-induced suppression of autoreactive T cell proliferation stimulated by syngeneic M phi. Dinoprostone 108-112 tumor necrosis factor Homo sapiens 81-90 7688311-4 1993 IL-10 further increased NO2- production by M phi stimulated in the presence of optimal concentrations of prostaglandin E2, a positive modulator of M phi activation by IFN-gamma/TNF-alpha. Dinoprostone 105-121 tumor necrosis factor Homo sapiens 177-186 8244447-10 1993 A PGE2-specific enzyme-linked immunosorbent assay showed that TBH M phi T cell cultures contained significantly more PGE2 than those containing NH M phi, and that exogenous TNF-alpha increased PGE2 production in TBH M phi cultures more than in NH M phi cultures. Dinoprostone 2-6 tumor necrosis factor Homo sapiens 173-182 8244447-10 1993 A PGE2-specific enzyme-linked immunosorbent assay showed that TBH M phi T cell cultures contained significantly more PGE2 than those containing NH M phi, and that exogenous TNF-alpha increased PGE2 production in TBH M phi cultures more than in NH M phi cultures. Dinoprostone 117-121 tumor necrosis factor Homo sapiens 173-182 8244447-4 1993 Because M phi produce tumor necrosis factor-alpha (TNF-alpha) during cancer, and TNF-alpha stimulates M phi PGE2 synthesis, we determined if TNF-alpha mediates tumor-induced suppression of autoreactive T cell proliferation stimulated by syngeneic M phi. Dinoprostone 108-112 tumor necrosis factor Homo sapiens 81-90 8244447-10 1993 A PGE2-specific enzyme-linked immunosorbent assay showed that TBH M phi T cell cultures contained significantly more PGE2 than those containing NH M phi, and that exogenous TNF-alpha increased PGE2 production in TBH M phi cultures more than in NH M phi cultures. Dinoprostone 117-121 tumor necrosis factor Homo sapiens 173-182 8244447-13 1993 Although TNF-alpha is known to increase T cell proliferation, these results show that the tumor-induced increase in M phi TNF-alpha synthesis suppress autoreactive T cell proliferation, which is mediated by PGE2 production. Dinoprostone 207-211 tumor necrosis factor Homo sapiens 9-18 8219674-3 1993 The results showed that as the level of plasma LPS raised the serum TNF, plasma PGE2 elevated obviously and the cellular immunity inhibited elevated in treatment and control groups. Dinoprostone 80-84 tumor necrosis factor Homo sapiens 68-71 8244447-13 1993 Although TNF-alpha is known to increase T cell proliferation, these results show that the tumor-induced increase in M phi TNF-alpha synthesis suppress autoreactive T cell proliferation, which is mediated by PGE2 production. Dinoprostone 207-211 tumor necrosis factor Homo sapiens 122-131 7683676-1 1993 We investigated the participation of prostaglandin (PG) E2 in the regulation of the alpha 1(I) procollagen gene expression by tumor necrosis factor alpha (TNF alpha), and interleukin-1 beta (IL-1 beta) in normal adult human lung fibroblasts. Dinoprostone 37-58 tumor necrosis factor Homo sapiens 126-153 7683676-1 1993 We investigated the participation of prostaglandin (PG) E2 in the regulation of the alpha 1(I) procollagen gene expression by tumor necrosis factor alpha (TNF alpha), and interleukin-1 beta (IL-1 beta) in normal adult human lung fibroblasts. Dinoprostone 37-58 tumor necrosis factor Homo sapiens 155-164 7683676-2 1993 TNF alpha (100 units/ml) and IL-1 beta (100 units/ml) stimulated the production of PGE2 and caused a dose-dependent inhibition of up to 54 and 66%, respectively, of the production of type I procollagen. Dinoprostone 83-87 tumor necrosis factor Homo sapiens 0-9 7683676-8 1993 These results indicate that TNF alpha and IL-1 beta inhibit the expression of the alpha 1(I) procollagen gene in human lung fibroblasts at the transcriptional level by a PGE2-independent effect as well as through the effect of endogenous fibroblast PGE2 released under the stimulus of the cytokines. Dinoprostone 170-174 tumor necrosis factor Homo sapiens 28-37 7683676-8 1993 These results indicate that TNF alpha and IL-1 beta inhibit the expression of the alpha 1(I) procollagen gene in human lung fibroblasts at the transcriptional level by a PGE2-independent effect as well as through the effect of endogenous fibroblast PGE2 released under the stimulus of the cytokines. Dinoprostone 249-253 tumor necrosis factor Homo sapiens 28-37 8360594-8 1993 A PGE2-specific enzyme-linked immunosorbent assay showed that TNF-alpha addition increased PGE2 production in NH m phi-containing cultures to that of TBH m phi-containing cultures. Dinoprostone 2-6 tumor necrosis factor Homo sapiens 62-71 8360594-8 1993 A PGE2-specific enzyme-linked immunosorbent assay showed that TNF-alpha addition increased PGE2 production in NH m phi-containing cultures to that of TBH m phi-containing cultures. Dinoprostone 91-95 tumor necrosis factor Homo sapiens 62-71 8360594-9 1993 Exogenous PGE2 did not affect the TNF-alpha enhancement of T cell proliferation without m phi s. Therefore, suppression induced by TNF-alpha was caused by increased m phi PGE2 production and not by TNF-alpha in concert with PGE2. Dinoprostone 10-14 tumor necrosis factor Homo sapiens 131-140 8360594-9 1993 Exogenous PGE2 did not affect the TNF-alpha enhancement of T cell proliferation without m phi s. Therefore, suppression induced by TNF-alpha was caused by increased m phi PGE2 production and not by TNF-alpha in concert with PGE2. Dinoprostone 10-14 tumor necrosis factor Homo sapiens 131-140 8360594-9 1993 Exogenous PGE2 did not affect the TNF-alpha enhancement of T cell proliferation without m phi s. Therefore, suppression induced by TNF-alpha was caused by increased m phi PGE2 production and not by TNF-alpha in concert with PGE2. Dinoprostone 171-175 tumor necrosis factor Homo sapiens 131-140 8360594-9 1993 Exogenous PGE2 did not affect the TNF-alpha enhancement of T cell proliferation without m phi s. Therefore, suppression induced by TNF-alpha was caused by increased m phi PGE2 production and not by TNF-alpha in concert with PGE2. Dinoprostone 171-175 tumor necrosis factor Homo sapiens 131-140 8360594-9 1993 Exogenous PGE2 did not affect the TNF-alpha enhancement of T cell proliferation without m phi s. Therefore, suppression induced by TNF-alpha was caused by increased m phi PGE2 production and not by TNF-alpha in concert with PGE2. Dinoprostone 171-175 tumor necrosis factor Homo sapiens 131-140 8360594-9 1993 Exogenous PGE2 did not affect the TNF-alpha enhancement of T cell proliferation without m phi s. Therefore, suppression induced by TNF-alpha was caused by increased m phi PGE2 production and not by TNF-alpha in concert with PGE2. Dinoprostone 171-175 tumor necrosis factor Homo sapiens 131-140 8387095-2 1993 In this study, cis-urocanic acid suppressed human monocyte production of TNF-alpha by a PGE2-dependent mechanism. Dinoprostone 88-92 tumor necrosis factor Homo sapiens 73-82 8218931-2 1993 IL-1 alpha, IL-1 beta and TNF-alpha, but not EGF nor TGF-alpha, stimulated prostaglandin E2 (PGE2) formation in the gingival fibroblasts. Dinoprostone 75-91 tumor necrosis factor Homo sapiens 26-35 8218931-2 1993 IL-1 alpha, IL-1 beta and TNF-alpha, but not EGF nor TGF-alpha, stimulated prostaglandin E2 (PGE2) formation in the gingival fibroblasts. Dinoprostone 93-97 tumor necrosis factor Homo sapiens 26-35 8218931-3 1993 The effect of IL-1 alpha, IL-1 beta and TNF-alpha on PGE2 formation was significantly potentiated by EGF in a dose-dependent manner. Dinoprostone 53-57 tumor necrosis factor Homo sapiens 40-49 8218931-9 1993 Data indicates that EGF potentiates the IL-1 and TNF-alpha induced PGE2 formation at the level of prostaglandin endoperoxide synthase (cyclooxygenase). Dinoprostone 67-71 tumor necrosis factor Homo sapiens 49-58 8457602-2 1993 Tumor necrosis factor (TNF) and interleukin-1 (IL-1) synergistically stimulate the production of prostaglandin E2 (PGE2) by amnion cells. Dinoprostone 97-113 tumor necrosis factor Homo sapiens 0-21 8388910-10 1993 A PGE2-specific enzyme-linked immunosorbent assay showed that PGE2 production was greater in Ia- m phi- than in WP m phi-containing cultures and greatest in cultures containing TBH Ia- m phi s. Because TNF-alpha enhances T cell responses, its effects on Ia- m phi PGE2-mediated suppression was determined. Dinoprostone 62-66 tumor necrosis factor Homo sapiens 202-211 8388910-10 1993 A PGE2-specific enzyme-linked immunosorbent assay showed that PGE2 production was greater in Ia- m phi- than in WP m phi-containing cultures and greatest in cultures containing TBH Ia- m phi s. Because TNF-alpha enhances T cell responses, its effects on Ia- m phi PGE2-mediated suppression was determined. Dinoprostone 62-66 tumor necrosis factor Homo sapiens 202-211 8388910-12 1993 However, inhibiting PGE2 production allowed TNF-alpha to stimulate T cell proliferation in TBH Ia- m phi-containing cultures. Dinoprostone 20-24 tumor necrosis factor Homo sapiens 44-53 8388910-14 1993 TNF-alpha not only mediates cytotoxicity but also counteracts Ia- m phi PGE2-mediated suppression. Dinoprostone 72-76 tumor necrosis factor Homo sapiens 0-9 8388910-15 1993 Although tumor growth increases Ia- m phi TNF-alpha production, enhanced PGE2 production blocks TNF-alpha"s stimulatory action on Ia- m phi s, which favors their suppressor function during tumor growth. Dinoprostone 73-77 tumor necrosis factor Homo sapiens 96-105 8457602-2 1993 Tumor necrosis factor (TNF) and interleukin-1 (IL-1) synergistically stimulate the production of prostaglandin E2 (PGE2) by amnion cells. Dinoprostone 97-113 tumor necrosis factor Homo sapiens 23-26 8457602-2 1993 Tumor necrosis factor (TNF) and interleukin-1 (IL-1) synergistically stimulate the production of prostaglandin E2 (PGE2) by amnion cells. Dinoprostone 115-119 tumor necrosis factor Homo sapiens 0-21 8457602-2 1993 Tumor necrosis factor (TNF) and interleukin-1 (IL-1) synergistically stimulate the production of prostaglandin E2 (PGE2) by amnion cells. Dinoprostone 115-119 tumor necrosis factor Homo sapiens 23-26 7506004-6 1993 In contrast, PGE2, which significantly elevated intracellular cAMP levels, inhibited TNF but not IL-1 production at the transcriptional level. Dinoprostone 13-17 tumor necrosis factor Homo sapiens 85-88 8384689-0 1993 Fibroblast growth factor increases TNF alpha-mediated prostaglandin E2 production and TNF alpha receptor expression in human fibroblasts. Dinoprostone 54-70 tumor necrosis factor Homo sapiens 35-44 8384689-1 1993 To examine the possible role of basic fibroblast growth factor (FGF) in regulating the effects of TNF alpha, we tested the effect of FGF on TNF alpha-mediated PGE2 production and TNF alpha receptor expression in human fibroblasts. Dinoprostone 159-163 tumor necrosis factor Homo sapiens 140-149 8384689-1 1993 To examine the possible role of basic fibroblast growth factor (FGF) in regulating the effects of TNF alpha, we tested the effect of FGF on TNF alpha-mediated PGE2 production and TNF alpha receptor expression in human fibroblasts. Dinoprostone 159-163 tumor necrosis factor Homo sapiens 140-149 8384689-2 1993 We found that, while FGF alone had no effect on PGE2 production, it enhanced the amount of PGE2 produced in response to TNF alpha between 3 and 11-fold. Dinoprostone 91-95 tumor necrosis factor Homo sapiens 120-129 8384689-3 1993 FGF stimulated TNF alpha-induced PGE2 production independent of potential TNF alpha-mediated IL-1 production, as neither anti-IL-1 mAbs nor IL-1 receptor antagonist protein (IRAP) inhibited TNF alpha induced-PGE2 production or the stimulatory effect of FGF. Dinoprostone 33-37 tumor necrosis factor Homo sapiens 15-24 8384689-4 1993 A one minute exposure of cells to FGF prior to removal was sufficient to significantly enhance TNF alpha-induced PGE2 production; the maximal FGF effect was reached after a 6 h preincubation. Dinoprostone 113-117 tumor necrosis factor Homo sapiens 95-104 8384689-7 1993 The FGF-mediated increase in TNF alpha receptor expression and TNF alpha-mediated PGE2 production could be abolished by FGF mAbs, indicating a specific FGF effect. Dinoprostone 82-86 tumor necrosis factor Homo sapiens 63-72 8384689-8 1993 These results show that FGF increases TNF alpha receptor expression and suggest that this may account, at least in part, for the ability of FGF to enhance TNF alpha-mediated PGE2 production in human fibroblasts. Dinoprostone 174-178 tumor necrosis factor Homo sapiens 38-47 8384689-8 1993 These results show that FGF increases TNF alpha receptor expression and suggest that this may account, at least in part, for the ability of FGF to enhance TNF alpha-mediated PGE2 production in human fibroblasts. Dinoprostone 174-178 tumor necrosis factor Homo sapiens 155-164 8360707-10 1993 Whereas the levels of PGE2 in TNF-susceptible cell lines, H-4 and SF-188, were higher than those of other lines. Dinoprostone 22-26 tumor necrosis factor Homo sapiens 30-33 8492010-2 1993 The results were as follows: 1) TNF alpha enhanced the production of MMPs and PGE2 and suppressed TIMP production. Dinoprostone 78-82 tumor necrosis factor Homo sapiens 32-41 8341137-6 1993 TNF alpha (> or = 1 ng/ml) significantly stimulated the biosynthesis of PGE2 by a process that was also potentiated by p-HPPH. Dinoprostone 75-79 tumor necrosis factor Homo sapiens 0-9 8392688-2 1993 Massive liberation of bacterial cell wall components (Lipopolysaccharide, acid teichoic polymers) induce a cascade of reactions including the secretion of many cytokines (such as TNF alpha and IL-1 beta) and prostaglandins (such as PAF and PGE2) which in turn leads to the development of cerebral oedema, intracranial hypertension and cerebral blood flow reduction. Dinoprostone 240-244 tumor necrosis factor Homo sapiens 179-188 8341137-2 1993 IL-1 alpha, IL-1 beta and TNF alpha, dose-dependently, stimulated PGE2 formation in gingival fibroblasts. Dinoprostone 66-70 tumor necrosis factor Homo sapiens 26-35 1458686-6 1992 Experiments with combinations of recombinant mouse IFN-gamma and human lymphotoxin or TNF-alpha showed that these lymphokines could substitute for the direct T lymphocyte effects causing a synergistic growth inhibition and PGE2 release from mouse MC. Dinoprostone 223-227 tumor necrosis factor Homo sapiens 86-95 1632769-3 1992 However, exogenous PGE2 at the levels induced by TNF is not sufficient to affect lipolysis or LPL activity and low doses of indomethacin and flurbiprofen block PG production without affecting TNF"s action. Dinoprostone 19-23 tumor necrosis factor Homo sapiens 49-52 1410528-4 1992 EGF, IL-1 beta and TNF-alpha alone caused a dose-dependent increase in PGE2 production, while IL-6, IL-8 and GM-CSF were ineffective over the dose range tested. Dinoprostone 71-75 tumor necrosis factor Homo sapiens 19-28 1410528-5 1992 When cells were preincubated with IL-1 beta or TNF-alpha, there was a dose-dependent potentiation of EGF-induced PGE2 production that was greater than the sum of EGF alone and IL-1 beta or TNF-alpha alone. Dinoprostone 113-117 tumor necrosis factor Homo sapiens 47-56 1410528-6 1992 In each case, the minimum dose of IL-1 beta or TNF-alpha which amplified EGF-induced PGE2 production was 0.1 ng/ml (p less than 0.05, Student"s t-test). Dinoprostone 85-89 tumor necrosis factor Homo sapiens 47-56 1410528-7 1992 These data show that low concentrations of IL-1 beta or TNF-alpha may serve to amplify EGF-mediated PGE2 biosynthesis in amnion-derived cells and suggest that cytokines may modulate EGF function in responsive cells. Dinoprostone 100-104 tumor necrosis factor Homo sapiens 56-65 1322806-5 1992 Neutral proteinase and PGE2 production by BNC was also induced by TNF alpha (0.2-200 ng/ml) in a time-dependent (0-72 hr) manner. Dinoprostone 23-27 tumor necrosis factor Homo sapiens 66-75 1442930-7 1992 RESULTS: Transforming growth factor-beta decreased the interleukin-1- or tumor necrosis factor-induced prostaglandin E2 production by 70% to 80% and the basal prostaglandin E2 synthesis by 27%. Dinoprostone 103-119 tumor necrosis factor Homo sapiens 73-94 1504741-10 1992 TNF-alpha (greater than or equal to 0.01 micrograms ml-1) significantly stimulated the biosynthesis of PGE2 by a process that was potentiated by PHT. Dinoprostone 103-107 tumor necrosis factor Homo sapiens 0-9 1442930-7 1992 RESULTS: Transforming growth factor-beta decreased the interleukin-1- or tumor necrosis factor-induced prostaglandin E2 production by 70% to 80% and the basal prostaglandin E2 synthesis by 27%. Dinoprostone 159-175 tumor necrosis factor Homo sapiens 73-94 1442930-8 1992 The synergistic stimulation of prostaglandin E2 production by the combination of interleukin-1 with tumor necrosis factor was inhibited by 80% in cells treated with transforming growth factor-beta. Dinoprostone 31-47 tumor necrosis factor Homo sapiens 100-121 1548034-0 1992 Prostaglandin E2 inhibits the release of tumor necrosis factor-alpha, rather than interleukin 1 beta, from human macrophages. Dinoprostone 0-16 tumor necrosis factor Homo sapiens 41-68 1427594-3 1992 TNF at a low dose (10 U/ml) stimulated production of prostaglandin E2, Mn-superoxide dismutase, interleukin (IL)-6 and IL-8 by glioblastoma cells. Dinoprostone 53-69 tumor necrosis factor Homo sapiens 0-3 1548034-6 1992 In peritoneal macrophages collected during an infection-free period, TNF alpha release decreased from 3225 pg/ml (controls) to 353 pg/ml at 1000 ng/ml of PGE2, and in peritoneal macrophages collected during an episode of infectious peritonitis, it decreased from 4100 pg/ml (controls) to 545 pg/ml at 100 ng/ml of PGE2. Dinoprostone 154-158 tumor necrosis factor Homo sapiens 69-78 1501156-3 1992 In fibroblasts, derived after 9 months of PHT therapy, IL-1 alpha, IL-1 beta and TNF alpha induced a significantly higher formation of PGE2 compared to that in fibroblasts derived before PHT therapy. Dinoprostone 135-139 tumor necrosis factor Homo sapiens 81-90 1548034-5 1992 We found that PGE2 invariably induced a dose-dependent decrease in TNF alpha release. Dinoprostone 14-18 tumor necrosis factor Homo sapiens 67-76 1548034-6 1992 In peritoneal macrophages collected during an infection-free period, TNF alpha release decreased from 3225 pg/ml (controls) to 353 pg/ml at 1000 ng/ml of PGE2, and in peritoneal macrophages collected during an episode of infectious peritonitis, it decreased from 4100 pg/ml (controls) to 545 pg/ml at 100 ng/ml of PGE2. Dinoprostone 314-318 tumor necrosis factor Homo sapiens 69-78 1658153-7 1991 In contrast, NMA enhances the synthesis of both gelatinase and PGE2 after activation with a combination of IL-1, LPS, and TNF-alpha. Dinoprostone 63-67 tumor necrosis factor Homo sapiens 122-131 1548034-10 1992 These findings indicate that exogenous and endogenous PGE2 controls the release of TNF alpha rather than IL-1 beta from LPS-stimulated peritoneal macrophages. Dinoprostone 54-58 tumor necrosis factor Homo sapiens 83-92 1480760-2 1992 It is produced by the actions of circulating cytokines, such as interleukin-1 (IL-1) and tumor necrosis factor (TNF), on the organum vasculosum of the lamina terminalis (OVLT), resulting in the secretion of prostaglandin E2, which initiates a variety of responses, including elevation of body temperature and corticosteroid secretion. Dinoprostone 207-223 tumor necrosis factor Homo sapiens 89-110 1480760-2 1992 It is produced by the actions of circulating cytokines, such as interleukin-1 (IL-1) and tumor necrosis factor (TNF), on the organum vasculosum of the lamina terminalis (OVLT), resulting in the secretion of prostaglandin E2, which initiates a variety of responses, including elevation of body temperature and corticosteroid secretion. Dinoprostone 207-223 tumor necrosis factor Homo sapiens 112-115 1752317-3 1991 Late (DS1.1+) CFU-GM displayed the highest sensitivity to PGE2 and TNF alpha, the first significant inhibition being evident at 10(-9)M PGE2 and 1 U/ml TNF alpha. Dinoprostone 58-62 tumor necrosis factor Homo sapiens 152-161 1752317-3 1991 Late (DS1.1+) CFU-GM displayed the highest sensitivity to PGE2 and TNF alpha, the first significant inhibition being evident at 10(-9)M PGE2 and 1 U/ml TNF alpha. Dinoprostone 136-140 tumor necrosis factor Homo sapiens 67-76 1836009-5 1991 We found that sphingosine enhanced TNF alpha-induced PGE2 production by as much as 18-fold over TNF alpha alone. Dinoprostone 53-57 tumor necrosis factor Homo sapiens 35-44 1455368-6 1992 The RA patients demonstrated direct correlations between the level of IL-1 beta, TNF-alpha and PGE2 in supernatants of PBM, whereas the donors showed up a negative correlation between IL-1 beta activity and PGE2. Dinoprostone 95-99 tumor necrosis factor Homo sapiens 81-90 1836009-0 1991 Sphingosine synergistically stimulates tumor necrosis factor alpha-induced prostaglandin E2 production in human fibroblasts. Dinoprostone 75-91 tumor necrosis factor Homo sapiens 39-66 1836009-12 1991 It appears that sphingosine affects TNF alpha-induced PGE2 production via a mechanism that is independent of PKC involvement, and that sphingosine may function as an endogenous second messenger capable of modulating the responsiveness of the cell to external stimuli. Dinoprostone 54-58 tumor necrosis factor Homo sapiens 36-45 1836009-4 1991 Because TNF alpha is known to induce prostaglandin E2 (PGE2) production in human fibroblasts, we tested the effect of sphingosine on TNF alpha-induced PGE2 production. Dinoprostone 37-53 tumor necrosis factor Homo sapiens 8-17 1836009-4 1991 Because TNF alpha is known to induce prostaglandin E2 (PGE2) production in human fibroblasts, we tested the effect of sphingosine on TNF alpha-induced PGE2 production. Dinoprostone 55-59 tumor necrosis factor Homo sapiens 8-17 1836009-4 1991 Because TNF alpha is known to induce prostaglandin E2 (PGE2) production in human fibroblasts, we tested the effect of sphingosine on TNF alpha-induced PGE2 production. Dinoprostone 151-155 tumor necrosis factor Homo sapiens 133-142 1836009-5 1991 We found that sphingosine enhanced TNF alpha-induced PGE2 production by as much as 18-fold over TNF alpha alone. Dinoprostone 53-57 tumor necrosis factor Homo sapiens 96-105 1836009-6 1991 Sphingosine appeared to stimulate TNF alpha-induced PGE2 production independent of TNF alpha-mediated interleukin 1 (IL-1) production, because anti-IL-1 antibodies and IL-1 receptor antagonist protein (IRAP) did not inhibit TNF alpha-induced PGE2 production or the stimulatory effect of sphingosine. Dinoprostone 52-56 tumor necrosis factor Homo sapiens 34-43 1836009-7 1991 TNF alpha stimulated PGE2 production to the same degree in normal and protein kinase C (PKC) downregulated cells in the presence and absence of sphingosine, indicating that neither TNF alpha nor sphingosine require active PKC to elicit their respective effects. Dinoprostone 21-25 tumor necrosis factor Homo sapiens 0-9 1836009-9 1991 Short-term (1 min) exposure of cells to sphingosine dramatically increased TNF alpha-induced PGE2 production. Dinoprostone 93-97 tumor necrosis factor Homo sapiens 75-84 1836009-10 1991 A potential mechanism by which sphingosine could increase TNF alpha-induced PGE2 production involves enhancement of phospholipase A2 (PLA2) and/or cyclooxygenase (Cox) activity, the rate-limiting enzymes in PGE2 production. Dinoprostone 76-80 tumor necrosis factor Homo sapiens 58-67 1836009-10 1991 A potential mechanism by which sphingosine could increase TNF alpha-induced PGE2 production involves enhancement of phospholipase A2 (PLA2) and/or cyclooxygenase (Cox) activity, the rate-limiting enzymes in PGE2 production. Dinoprostone 207-211 tumor necrosis factor Homo sapiens 58-67 1930911-4 1991 IL-1, IL-6 and TNF-alpha have several functions which suggest that they participate in the chronic disease process of rheumatoid arthritis, such as increasing production of eicosanoid, collagenase and prostaglandin E2. Dinoprostone 201-217 tumor necrosis factor Homo sapiens 15-24 1815239-1 1991 We examined the interactions between supernatant from FMLP-activated human granulocytes, recombinant interleukin-1 (IL-1) and recombinant tumor necrosis factor (TNF) in the stimulation of prostaglandin E2 (PGE2) production by human amnion cells. Dinoprostone 188-204 tumor necrosis factor Homo sapiens 138-159 1815239-1 1991 We examined the interactions between supernatant from FMLP-activated human granulocytes, recombinant interleukin-1 (IL-1) and recombinant tumor necrosis factor (TNF) in the stimulation of prostaglandin E2 (PGE2) production by human amnion cells. Dinoprostone 188-204 tumor necrosis factor Homo sapiens 161-164 1815239-1 1991 We examined the interactions between supernatant from FMLP-activated human granulocytes, recombinant interleukin-1 (IL-1) and recombinant tumor necrosis factor (TNF) in the stimulation of prostaglandin E2 (PGE2) production by human amnion cells. Dinoprostone 206-210 tumor necrosis factor Homo sapiens 161-164 1815239-7 1991 The combinations of IL-1 alpha or IL-1 beta with either TNF-alpha or TNF-beta caused a synergistic stimulation of amnion cell PGE2 production as well, whereas the combinations of IL-1 alpha with IL-1 beta or of TNF-alpha with TNF-beta were not synergistic. Dinoprostone 126-130 tumor necrosis factor Homo sapiens 56-65 1815239-8 1991 Furthermore, granulocyte supernatant was synergistic with the combination of IL-1 and TNF, resulting in a more than 150-fold stimulation of PGE2 production. Dinoprostone 140-144 tumor necrosis factor Homo sapiens 86-89 1815239-10 1991 We propose that granulocyte products acting together with IL-1 and TNF enhance PGE2 synthesis during inflammation, and serve as signals for the initiation of preterm labor in the setting of intra-amniotic infection. Dinoprostone 79-83 tumor necrosis factor Homo sapiens 67-70 1773338-2 1991 The cytokines, interleukin-1 (IL-1) and tumor necrosis factor (TNF), are two pyrogens which stimulate brain PGE2 formation during fever and also increase PGE2 synthesis in human mononuclear cells in vitro. Dinoprostone 108-112 tumor necrosis factor Homo sapiens 40-61 1773338-2 1991 The cytokines, interleukin-1 (IL-1) and tumor necrosis factor (TNF), are two pyrogens which stimulate brain PGE2 formation during fever and also increase PGE2 synthesis in human mononuclear cells in vitro. Dinoprostone 108-112 tumor necrosis factor Homo sapiens 63-66 1773338-2 1991 The cytokines, interleukin-1 (IL-1) and tumor necrosis factor (TNF), are two pyrogens which stimulate brain PGE2 formation during fever and also increase PGE2 synthesis in human mononuclear cells in vitro. Dinoprostone 154-158 tumor necrosis factor Homo sapiens 40-61 1773338-2 1991 The cytokines, interleukin-1 (IL-1) and tumor necrosis factor (TNF), are two pyrogens which stimulate brain PGE2 formation during fever and also increase PGE2 synthesis in human mononuclear cells in vitro. Dinoprostone 154-158 tumor necrosis factor Homo sapiens 63-66 1659380-2 1991 Cultivation of differentiated HL-60 cells with 100 units of TNF/ml for 24 h resulted in a 3-fold increase in superoxide release and 4-fold increase in prostaglandin E2 production on stimulation with 1 microM-FMLP. Dinoprostone 151-167 tumor necrosis factor Homo sapiens 60-63 1717193-5 1991 ATRA inhibited both IL-1 beta- and TNF alpha-induced secretion of prostaglandin-E2 (PGE2), a potent feedback inhibitor of cytokine-stimulated HSN proliferation. Dinoprostone 66-82 tumor necrosis factor Homo sapiens 35-44 1717193-5 1991 ATRA inhibited both IL-1 beta- and TNF alpha-induced secretion of prostaglandin-E2 (PGE2), a potent feedback inhibitor of cytokine-stimulated HSN proliferation. Dinoprostone 84-88 tumor necrosis factor Homo sapiens 35-44 1858031-6 1991 When cyclooxygenase blockade with indomethacin completely prevented KC production of PGE2 in (-)arginine culture, TNF-alpha production was upregulated (p less than 0.001 vs (-)arginine; p not significant vs (+)arginine). Dinoprostone 85-89 tumor necrosis factor Homo sapiens 114-123 1858031-7 1991 These arginine-specific depression of TNF-alpha responses appeared unique to KC because both TNF-alpha and PGE2 levels increased when peritoneal, pleural, and alveolar macrophages were stimulated by lipopolysaccharide in (-)arginine medium. Dinoprostone 107-111 tumor necrosis factor Homo sapiens 38-47 1914496-3 1991 Gamma Interferon (gamma-IFN), Tumor Necrosis Factor (TNF), and Interleukin 1 (IL1) are peptide regulatory factors involved in immunological responses, but they also play a role in the synthesis of collagen and prostaglandin E2 by fibroblasts. Dinoprostone 210-226 tumor necrosis factor Homo sapiens 30-51 1858031-8 1991 This PGE2-dependent autoregulation of potentially harmful lipopolysaccharide-induced TNF-alpha responses may reflect an evolutionary adaptation by KC to their local hepatic environment and strategic anatomic position in the portal circuit, which optimally removes endotoxin and naturally protects the host. Dinoprostone 5-9 tumor necrosis factor Homo sapiens 85-94 1914496-3 1991 Gamma Interferon (gamma-IFN), Tumor Necrosis Factor (TNF), and Interleukin 1 (IL1) are peptide regulatory factors involved in immunological responses, but they also play a role in the synthesis of collagen and prostaglandin E2 by fibroblasts. Dinoprostone 210-226 tumor necrosis factor Homo sapiens 53-56 1893073-2 1991 Recombinant interleukin-1-beta (IL-1-beta) and tumor necrosis factor-alpha (TNF-alpha) stimulated moderately the DNA synthesis and markedly the production of PGE2. Dinoprostone 158-162 tumor necrosis factor Homo sapiens 47-74 1904465-2 1991 It is modulated by interferon-gamma, prostaglandin E2 and indomethacin in the same manner as observed with tumour necrosis factor (TNF) release from human monocyte/macrophage cells cultured in vitro. Dinoprostone 37-53 tumor necrosis factor Homo sapiens 131-134 1893073-2 1991 Recombinant interleukin-1-beta (IL-1-beta) and tumor necrosis factor-alpha (TNF-alpha) stimulated moderately the DNA synthesis and markedly the production of PGE2. Dinoprostone 158-162 tumor necrosis factor Homo sapiens 76-85 1893073-5 1991 Incubation with a crude T cell supernatant or a mixture of cytokines including IL-1-beta, TNF-alpha and IFN-gamma enhanced synovial cell growth and PGE2 production as compared to the effect elicited by each single cytokine. Dinoprostone 148-152 tumor necrosis factor Homo sapiens 90-99 1679130-12 1991 PGE2 exerts a control over the whole process by suppressing production of both IL-1 and TNF-alpha. Dinoprostone 0-4 tumor necrosis factor Homo sapiens 88-97 2068050-4 1991 The effects of indomethacin on TNF release and TNF gene expression were due to the inhibition of endogenous prostaglandin (PG)E2 production. Dinoprostone 108-128 tumor necrosis factor Homo sapiens 31-34 2068050-4 1991 The effects of indomethacin on TNF release and TNF gene expression were due to the inhibition of endogenous prostaglandin (PG)E2 production. Dinoprostone 108-128 tumor necrosis factor Homo sapiens 47-50 2068050-7 1991 Exogenous PGE2 suppressed the release of TNF and the expression of TNF gene in a dose-dependent fashion. Dinoprostone 10-14 tumor necrosis factor Homo sapiens 41-44 2068050-7 1991 Exogenous PGE2 suppressed the release of TNF and the expression of TNF gene in a dose-dependent fashion. Dinoprostone 10-14 tumor necrosis factor Homo sapiens 67-70 2068050-8 1991 Exogenous PGE2 completely reversed the effects of indomethacin on TNF production at 24 h. These findings suggest that indomethacin may significantly alter the kinetics of TNF release and TNF gene expression by LPS-stimulated BM. Dinoprostone 10-14 tumor necrosis factor Homo sapiens 66-69 2068050-8 1991 Exogenous PGE2 completely reversed the effects of indomethacin on TNF production at 24 h. These findings suggest that indomethacin may significantly alter the kinetics of TNF release and TNF gene expression by LPS-stimulated BM. Dinoprostone 10-14 tumor necrosis factor Homo sapiens 171-174 2068050-8 1991 Exogenous PGE2 completely reversed the effects of indomethacin on TNF production at 24 h. These findings suggest that indomethacin may significantly alter the kinetics of TNF release and TNF gene expression by LPS-stimulated BM. Dinoprostone 10-14 tumor necrosis factor Homo sapiens 171-174 2068050-9 1991 These effects are related, at least in part, to the inhibition of the production of endogenous PGE2, an important self-driven regulatory factor of the kinetics of TNF production. Dinoprostone 95-99 tumor necrosis factor Homo sapiens 163-166 1651782-2 1991 Since IL-1 alpha, IL-1 beta and TNF alpha have been previously demonstrated to play an important role in connective tissue destruction by stimulating the production of prostaglandin E2 (PGE2) and collagenase, these functions were investigated in the presence or absence of natural human IL-6 (nhIL-6) or recombinant human IL-6 (rhIL-6). Dinoprostone 168-184 tumor necrosis factor Homo sapiens 32-41 1987772-9 1991 At both levels, however, TNF alpha caused increased release of both prostacyclin and PGE2. Dinoprostone 85-89 tumor necrosis factor Homo sapiens 25-34 1993070-8 1991 Cell growth stimulated by TNF and indomethacin was inhibited by exogenously added prostaglandins (PGE2, PGF2 alpha, and PGD2), among which PGE2 caused the greatest inhibition of cell growth. Dinoprostone 98-102 tumor necrosis factor Homo sapiens 26-29 1993070-8 1991 Cell growth stimulated by TNF and indomethacin was inhibited by exogenously added prostaglandins (PGE2, PGF2 alpha, and PGD2), among which PGE2 caused the greatest inhibition of cell growth. Dinoprostone 139-143 tumor necrosis factor Homo sapiens 26-29 1993070-9 1991 Treatment of FS-4 cells with 10 ng/ml TNF resulted in the release of prostaglandins (PGE2, 6-keto-PGF1 alpha, PGA2, PGD2, and PGF2 alpha) 2 to 4 fold over that of untreated cells. Dinoprostone 85-89 tumor necrosis factor Homo sapiens 38-41 1993070-11 1991 In both TNF-treated and control cells, PGE2 was released as the predominant prostaglandin. Dinoprostone 39-43 tumor necrosis factor Homo sapiens 8-11 1651782-2 1991 Since IL-1 alpha, IL-1 beta and TNF alpha have been previously demonstrated to play an important role in connective tissue destruction by stimulating the production of prostaglandin E2 (PGE2) and collagenase, these functions were investigated in the presence or absence of natural human IL-6 (nhIL-6) or recombinant human IL-6 (rhIL-6). Dinoprostone 186-190 tumor necrosis factor Homo sapiens 32-41 1651782-6 1991 On the contrary in 2/4 experiments TNF alpha-induced PGE2 production was increased (approximately 2 fold) by the addition of IL-6. Dinoprostone 53-57 tumor necrosis factor Homo sapiens 35-44 2240281-6 1990 Normal plasma was found to inhibit TNF-alpha-induced PGE2 release by 20-35%. Dinoprostone 53-57 tumor necrosis factor Homo sapiens 35-44 2258704-8 1990 These data further underscore the potential importance of TNF-alpha in modulating a variety of fibroblast functions, including chemotaxis and synthesis of collagen, glycosaminoglycans, interleukin 1 alpha (IL-1 alpha) and -beta, human histocompatibility leukocyte antigen A and B antigens, collagenase, prostaglandin E2, and IL-6. Dinoprostone 303-319 tumor necrosis factor Homo sapiens 58-67 2387094-4 1990 The increase of TNF-alpha production by PBMC from tuberculosis patients was associated with a comparatively weaker elevation of PGE2 synthesis which did not parallel fever or weight loss. Dinoprostone 128-132 tumor necrosis factor Homo sapiens 16-25 2116086-6 1990 Concentrations of PGE2 correlated significantly with PGI2, IL-1 beta, TNF, and lactate and inversely correlated with glucose concentrations in the first CSF specimens. Dinoprostone 18-22 tumor necrosis factor Homo sapiens 70-73 2119339-2 1990 In the infected cultures that were treated with TNF, high concentrations of prostaglandin E2(PGE2) were detected, exceeding by far the concentrations found in TNF-treated but uninfected cells or in infected cells that were not treated with TNF. Dinoprostone 76-92 tumor necrosis factor Homo sapiens 48-51 2119339-2 1990 In the infected cultures that were treated with TNF, high concentrations of prostaglandin E2(PGE2) were detected, exceeding by far the concentrations found in TNF-treated but uninfected cells or in infected cells that were not treated with TNF. Dinoprostone 93-97 tumor necrosis factor Homo sapiens 48-51 2119339-6 1990 Excessive formation of PGE2 by cells infected with chlamydiae and treated by TNF might be related to some of the complications associated with chlamydial infection. Dinoprostone 23-27 tumor necrosis factor Homo sapiens 77-80 1698632-8 1990 as an inducer it was possible to demonstrate that TNF-alpha production is regulated by prostaglandin E2; preincubation of the cells with prostaglandin E2 resulted in a reduced C.p.-mediated TNF-alpha production (p less than 0.001). Dinoprostone 87-103 tumor necrosis factor Homo sapiens 50-59 1698632-8 1990 as an inducer it was possible to demonstrate that TNF-alpha production is regulated by prostaglandin E2; preincubation of the cells with prostaglandin E2 resulted in a reduced C.p.-mediated TNF-alpha production (p less than 0.001). Dinoprostone 137-153 tumor necrosis factor Homo sapiens 50-59 1698632-8 1990 as an inducer it was possible to demonstrate that TNF-alpha production is regulated by prostaglandin E2; preincubation of the cells with prostaglandin E2 resulted in a reduced C.p.-mediated TNF-alpha production (p less than 0.001). Dinoprostone 137-153 tumor necrosis factor Homo sapiens 190-199 2113477-6 1990 The TNF-alpha INH blocked prostaglandin E2 production by dermal fibroblasts in a dose-dependent manner, providing evidence for antiinflammatory activity. Dinoprostone 26-42 tumor necrosis factor Homo sapiens 4-13 1716487-2 1990 In this study, we report the effects of prostaglandin E2 (PGE2), and two other cAMP-elevating agents, dibutyryl cAMP and 3-isobutyl-1-methyl-xanthine, on the in vitro LPS-induced production of IL 6, IL 1 alpha, IL 1 beta and TNF alpha by human monocytes. Dinoprostone 40-56 tumor necrosis factor Homo sapiens 225-234 1716487-8 1990 These results demonstrate that IL 6, TNF alpha, IL 1 alpha and IL 1 beta production can be differently modulated by an agent, PGE2, which is produced simultaneously by LPS-stimulated monocytes. Dinoprostone 126-130 tumor necrosis factor Homo sapiens 37-46 2156930-11 1990 Moreover, the cyclooxygenase metabolite, PGE2, as well as dibutyryl cAMP, inhibited the induction of TNF transcripts by LPS. Dinoprostone 41-45 tumor necrosis factor Homo sapiens 101-104 2334439-0 1990 Mononuclear cells enhance prostaglandin E2 production of polymorphonuclear leukocytes via tumor necrosis factor alpha. Dinoprostone 26-42 tumor necrosis factor Homo sapiens 90-117 2334439-3 1990 TNF alpha, but not IL-1, IL-2, IL-6, or IFN gamma, enhanced the prostaglandin E2 production when added in vitro. Dinoprostone 64-80 tumor necrosis factor Homo sapiens 0-9 2104744-0 1990 Elevated tumor necrosis factor alpha production concomitant to elevated prostaglandin E2 production by trauma patients" monocytes. Dinoprostone 72-88 tumor necrosis factor Homo sapiens 9-36 2319205-6 1990 TNF-alpha in doses greater than 500 ng/ml caused fibroblast death, probably by a prostaglandin related mechanism as fibroblasts remained viable, although non proliferative, when assayed in the presence of indomethacin, a known inhibitor of prostaglandin E2 (PGE2) synthesis. Dinoprostone 240-256 tumor necrosis factor Homo sapiens 0-9 2319205-6 1990 TNF-alpha in doses greater than 500 ng/ml caused fibroblast death, probably by a prostaglandin related mechanism as fibroblasts remained viable, although non proliferative, when assayed in the presence of indomethacin, a known inhibitor of prostaglandin E2 (PGE2) synthesis. Dinoprostone 258-262 tumor necrosis factor Homo sapiens 0-9 2319209-9 1990 Concomitant administration of LPS with either prostaglandin E2 (10(-6)M) or Dexamethasone (10(-6)M) resulted in significant suppression of LPS-induced TNF production. Dinoprostone 46-62 tumor necrosis factor Homo sapiens 151-154 1689760-7 1990 PGE-2 inhibits the secretion of CSFs and TNF. Dinoprostone 0-5 tumor necrosis factor Homo sapiens 41-44 1689760-10 1990 PGE-2 added with LPS during the 24-48 h induction blocks M-CSF and TNF production, but appears to enhance M-CSF message expression, in contrast to its effect on 0 h inductions. Dinoprostone 0-5 tumor necrosis factor Homo sapiens 67-70 2310781-5 1990 The increased PGE2 production by the chondrocytes exhibited a lag phase of 4-8 h following the addition of the IL-1 or TNF and was inhibited by actinomycin D and cycloheximide, indicating a requirement for de novo RNA and protein synthesis, respectively. Dinoprostone 14-18 tumor necrosis factor Homo sapiens 119-122 2137848-11 1990 Greater TNF production by the FcRI+ M phi subset was induced concomitant to elevation of its prostaglandin E2 production. Dinoprostone 93-109 tumor necrosis factor Homo sapiens 8-11 2178606-1 1990 The stimulation of the production of osteocalcin by human osteoblast-like cells in response to 1,25(OH)2D3 is antagonized by several agents that induce the synthesis of prostaglandin E2 (PGE2) including interleukin 1 (IL-1), tumour necrosis factor (TNF) and parathyroid hormone (PTH). Dinoprostone 169-185 tumor necrosis factor Homo sapiens 225-247 2178606-1 1990 The stimulation of the production of osteocalcin by human osteoblast-like cells in response to 1,25(OH)2D3 is antagonized by several agents that induce the synthesis of prostaglandin E2 (PGE2) including interleukin 1 (IL-1), tumour necrosis factor (TNF) and parathyroid hormone (PTH). Dinoprostone 169-185 tumor necrosis factor Homo sapiens 249-252 2178606-1 1990 The stimulation of the production of osteocalcin by human osteoblast-like cells in response to 1,25(OH)2D3 is antagonized by several agents that induce the synthesis of prostaglandin E2 (PGE2) including interleukin 1 (IL-1), tumour necrosis factor (TNF) and parathyroid hormone (PTH). Dinoprostone 187-191 tumor necrosis factor Homo sapiens 225-247 2178606-1 1990 The stimulation of the production of osteocalcin by human osteoblast-like cells in response to 1,25(OH)2D3 is antagonized by several agents that induce the synthesis of prostaglandin E2 (PGE2) including interleukin 1 (IL-1), tumour necrosis factor (TNF) and parathyroid hormone (PTH). Dinoprostone 187-191 tumor necrosis factor Homo sapiens 249-252 2110931-3 1990 Additionally, the effects of prostaglandin E2 (PGE2), dexamethasone (dex), and cyclosporine A (CsA) on TNF gene expression have been studied, although little is known of the effects these compounds have on TNF containing samples. Dinoprostone 29-45 tumor necrosis factor Homo sapiens 103-106 2105339-7 1990 PGE2 or dibutyryl cAMP treatment of HL-60 cells in the presence of TNF blocked the expression of CSF-1 mRNA in a dose-dependent manner. Dinoprostone 0-4 tumor necrosis factor Homo sapiens 67-70 2105339-8 1990 These findings suggest that the increase in CSF-1 RNA observed during TNF treatment is regulated, at least in part, by both transcriptional and posttranscriptional mechanisms, and that PGE2 and cAMP regulate transcriptional activation of the CSF-1 gene by TNF. Dinoprostone 185-189 tumor necrosis factor Homo sapiens 256-259 2378446-6 1990 Inhibition of PGE2 production by indomethacin resulted in increased production of TNF from rickettsial-infected MdM, while addition of PGE2 caused partial inhibition of TNF production from infected MdM. Dinoprostone 14-18 tumor necrosis factor Homo sapiens 82-85 2378446-6 1990 Inhibition of PGE2 production by indomethacin resulted in increased production of TNF from rickettsial-infected MdM, while addition of PGE2 caused partial inhibition of TNF production from infected MdM. Dinoprostone 135-139 tumor necrosis factor Homo sapiens 169-172 33776573-3 2021 More specifically, TNFalpha/IL-1beta promotes expression of the prostaglandin E2- (PGE2-) producing enzymes, cyclooxygenase-2 (COX-2) and microsomal prostaglandin E synthase-1 (mPGES-1). Dinoprostone 64-80 tumor necrosis factor Homo sapiens 19-27 33776573-3 2021 More specifically, TNFalpha/IL-1beta promotes expression of the prostaglandin E2- (PGE2-) producing enzymes, cyclooxygenase-2 (COX-2) and microsomal prostaglandin E synthase-1 (mPGES-1). Dinoprostone 83-87 tumor necrosis factor Homo sapiens 19-27 33776573-12 2021 Transient transfection of miR-708 suppressed TNFalpha/IL-1beta-induced changes in COX-2, mPGES-1, and PGE2 levels. Dinoprostone 102-106 tumor necrosis factor Homo sapiens 45-53 7880974-8 1994 Both p55 and p75 TNF receptors on dermal and gingival fibroblasts were also involved in TNF-alpha-mediated DNA synthesis and IL-6, IL-8 and PGE2 release, although differences in the levels of DNA synthesis and release of inflammatory cytokines and PGE2 were observed between the three fibroblast types. Dinoprostone 248-252 tumor necrosis factor Homo sapiens 88-97 7880974-6 1994 TNF-alpha-stimulated synovial fibroblast DNA synthesis and the release of IL-6, IL-8 and PGE2 was inhibited by antagonist monoclonal antibodies against either the p55 or the p75 TNF receptor, although the blockade of the p55 TNF receptor had a more potent effect than inhibition of the p75 TNF receptor alone. Dinoprostone 89-93 tumor necrosis factor Homo sapiens 0-9 34234507-0 2021 Upregulation of COX-2 and PGE2 Induced by TNF-alpha Mediated Through TNFR1/MitoROS/PKCalpha/P38 MAPK, JNK1/2/FoxO1 Cascade in Human Cardiac Fibroblasts. Dinoprostone 26-30 tumor necrosis factor Homo sapiens 42-51 34979377-8 2022 After co-cultivation of synoviocytes and TNF-alpha, the levels of Interleukin (IL)-8 and hyaluronic acid (HA) appeared a few changes, and those of chemotactic cytokine ligand (CCL) 2, CCL3, CCL5 and matrix metalloproteinases (MMP)-9 were downregulated, while the levels of Tissue Inhibitor of Metalloproteinases (TIMP)-1, IL-10 and Prostaglandin E2 (PGE2) were up-regulated. Dinoprostone 332-348 tumor necrosis factor Homo sapiens 41-50 34979377-8 2022 After co-cultivation of synoviocytes and TNF-alpha, the levels of Interleukin (IL)-8 and hyaluronic acid (HA) appeared a few changes, and those of chemotactic cytokine ligand (CCL) 2, CCL3, CCL5 and matrix metalloproteinases (MMP)-9 were downregulated, while the levels of Tissue Inhibitor of Metalloproteinases (TIMP)-1, IL-10 and Prostaglandin E2 (PGE2) were up-regulated. Dinoprostone 350-354 tumor necrosis factor Homo sapiens 41-50 34944517-3 2021 Paradoxically, PGE2 suppresses interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) production and triggers the production of lipoxin A4 (LXA4) from AA to initiate inflammation resolution process and augment regeneration of tissues. Dinoprostone 15-19 tumor necrosis factor Homo sapiens 56-83 34944517-3 2021 Paradoxically, PGE2 suppresses interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) production and triggers the production of lipoxin A4 (LXA4) from AA to initiate inflammation resolution process and augment regeneration of tissues. Dinoprostone 15-19 tumor necrosis factor Homo sapiens 85-94 34729107-0 2021 Anticancer Effects of Helminthostachys zeylanica Ethyl acetate Extracts on Human Gastric Cancer Cells through Downregulation of the TNF-alpha-activated COX-2-cPLA2-PGE2 Pathway. Dinoprostone 164-168 tumor necrosis factor Homo sapiens 132-141 34729107-9 2021 The anticancer effects of H. zeylanica-E2 in GC cells might be mediated partly through inhibition of tumor necrosis factor-alpha (TNF-alpha)-activated proinflammatory cytosolic phospholipase A2 (cPLA2)-COX-2-prostaglandin E2 (PGE2) pathway. Dinoprostone 208-224 tumor necrosis factor Homo sapiens 130-139 34729107-9 2021 The anticancer effects of H. zeylanica-E2 in GC cells might be mediated partly through inhibition of tumor necrosis factor-alpha (TNF-alpha)-activated proinflammatory cytosolic phospholipase A2 (cPLA2)-COX-2-prostaglandin E2 (PGE2) pathway. Dinoprostone 226-230 tumor necrosis factor Homo sapiens 130-139 34465013-6 2022 The concentration of PGE2 in FET colon cancer cells was measured both in the initial status and after stimulation by tumor necrosis factor (TNF)-alpha. Dinoprostone 21-25 tumor necrosis factor Homo sapiens 117-150 34465013-10 2022 In colon cancer cells, PGE2 was found to be upregulated upon stimulation by TNF-alpha, which led to strong induction of mPGES-1 without any change in the expression of COX-2 among the PGE2-related enzymes. Dinoprostone 23-27 tumor necrosis factor Homo sapiens 76-85 34465013-10 2022 In colon cancer cells, PGE2 was found to be upregulated upon stimulation by TNF-alpha, which led to strong induction of mPGES-1 without any change in the expression of COX-2 among the PGE2-related enzymes. Dinoprostone 184-188 tumor necrosis factor Homo sapiens 76-85 34465013-11 2022 Conclusion: These results demonstrated that PGE2 can be induced by stimuli such as TNF-alpha, and suggest that activation of mPGES-1 is more closely related than that of COX-2 in the induction of PGE2 on colon cancer. Dinoprostone 44-48 tumor necrosis factor Homo sapiens 83-92 34465013-11 2022 Conclusion: These results demonstrated that PGE2 can be induced by stimuli such as TNF-alpha, and suggest that activation of mPGES-1 is more closely related than that of COX-2 in the induction of PGE2 on colon cancer. Dinoprostone 196-200 tumor necrosis factor Homo sapiens 83-92 34234507-13 2021 Conclusion: Our results suggested that TNF-alpha-induced COX-2/PGE2 upregulation is mediated through TNFR1-dependent MitoROS/PKCalpha/p38 MAPK and JNK1/2 cascade to activate FoxO1 binding with the COX-2 promoter in HCFs. Dinoprostone 63-67 tumor necrosis factor Homo sapiens 39-48 34234507-1 2021 Purpose: Tumor necrosis factor-alpha (TNF-alpha) has been shown to exert as a pathogenic factor in cardiac fibrosis and heart failure which were associated with the up-regulation of cyclooxygenase (COX)-2/prostaglandin E2 (PGE2) axis. Dinoprostone 205-221 tumor necrosis factor Homo sapiens 9-36 34234507-1 2021 Purpose: Tumor necrosis factor-alpha (TNF-alpha) has been shown to exert as a pathogenic factor in cardiac fibrosis and heart failure which were associated with the up-regulation of cyclooxygenase (COX)-2/prostaglandin E2 (PGE2) axis. Dinoprostone 205-221 tumor necrosis factor Homo sapiens 38-47 34234507-1 2021 Purpose: Tumor necrosis factor-alpha (TNF-alpha) has been shown to exert as a pathogenic factor in cardiac fibrosis and heart failure which were associated with the up-regulation of cyclooxygenase (COX)-2/prostaglandin E2 (PGE2) axis. Dinoprostone 223-227 tumor necrosis factor Homo sapiens 9-36 34234507-1 2021 Purpose: Tumor necrosis factor-alpha (TNF-alpha) has been shown to exert as a pathogenic factor in cardiac fibrosis and heart failure which were associated with the up-regulation of cyclooxygenase (COX)-2/prostaglandin E2 (PGE2) axis. Dinoprostone 223-227 tumor necrosis factor Homo sapiens 38-47 34234507-2 2021 However, whether TNF-alpha-induced COX-2/PGE2 upregulation mediated through ROS-dependent cascade remains elusive in human cardiac fibroblasts (HCFs). Dinoprostone 41-45 tumor necrosis factor Homo sapiens 17-26 34234507-3 2021 This study aims to address the underlying mechanisms of TNF-alpha-induced COX-2/PGE2 expression. Dinoprostone 80-84 tumor necrosis factor Homo sapiens 56-65 35506586-0 2022 Orai2 channel regulates prostaglandin E2 production in TNFalpha/IL1alpha-stimulated astrocytes. Dinoprostone 24-40 tumor necrosis factor Homo sapiens 55-63 35506586-3 2022 In the present study, we found that astrocytes upregulate various inflammatory factors including prostaglandin E2 (PGE2 ) by co-stimulation with tumor necrosis factor-alpha (TNFalpha) and interleukin-1alpha (IL1alpha). Dinoprostone 97-113 tumor necrosis factor Homo sapiens 145-172 35506586-3 2022 In the present study, we found that astrocytes upregulate various inflammatory factors including prostaglandin E2 (PGE2 ) by co-stimulation with tumor necrosis factor-alpha (TNFalpha) and interleukin-1alpha (IL1alpha). Dinoprostone 97-113 tumor necrosis factor Homo sapiens 174-182 35506586-3 2022 In the present study, we found that astrocytes upregulate various inflammatory factors including prostaglandin E2 (PGE2 ) by co-stimulation with tumor necrosis factor-alpha (TNFalpha) and interleukin-1alpha (IL1alpha). Dinoprostone 115-119 tumor necrosis factor Homo sapiens 145-172 35506586-3 2022 In the present study, we found that astrocytes upregulate various inflammatory factors including prostaglandin E2 (PGE2 ) by co-stimulation with tumor necrosis factor-alpha (TNFalpha) and interleukin-1alpha (IL1alpha). Dinoprostone 115-119 tumor necrosis factor Homo sapiens 174-182 35506586-6 2022 The expression of the prostaglandin E synthase Ptges and the production of PGE2 were higher in Orai2-KD astrocytes than in WT astrocytes when stimulated with TNFalpha and IL1alpha. Dinoprostone 75-79 tumor necrosis factor Homo sapiens 158-166 35601817-4 2022 Another essential feature of hPDLSCs is their immunomodulatory activities, which are executed through cytokine (e.g., TNF-alpha and IL-1beta)-induced production of various soluble immunomediators (e.g., indoleamine-2,3-dioxygenase-1, tumor necrosis factor-inducible gene 6 protein, prostaglandin E2) and direct cell-to-cell contact (e.g., programmed cell death ligand 1, programmed cell death ligand 2). Dinoprostone 282-298 tumor necrosis factor Homo sapiens 118-127 35126344-10 2021 However, preventing prostaglandin E2 (PGE2) synthesis or blocking PGE2 binding to the cognate EP2/EP4 receptors, restored IFNgamma and TNFalpha production in OEC-conditioned T cells. Dinoprostone 66-70 tumor necrosis factor Homo sapiens 135-143 2550484-1 1989 Tumor necrosis factor stimulated prostaglandin E2 synthesis in Swiss 3T3 fibroblasts. Dinoprostone 33-49 tumor necrosis factor Homo sapiens 0-21 2804896-6 1989 As a result, in high-stage bladder cancer patients, there was a significant inverse correlation between TNF and PGE2 production of monocytes. Dinoprostone 112-116 tumor necrosis factor Homo sapiens 104-107 2801307-5 1989 Pretreatment with IL-1 or TNF dramatically amplified bradykinin-stimulated PGE2 synthesis. Dinoprostone 75-79 tumor necrosis factor Homo sapiens 26-29 2473844-7 1989 The secretion of TNF by rheumatoid synovial fluid mononuclear cells was inhibited by PGE2, while IFN-gamma enhanced its production in those cells which were spontaneously secreting TNF. Dinoprostone 85-89 tumor necrosis factor Homo sapiens 17-20 2787354-5 1989 Purified human rIL-1 alpha and IL-1 beta increased the levels of both products in the supernatants of the synovial cells; TNF-alpha raised the PGE2 levels but raised the plasminogen activator activity only weakly and inconsistently. Dinoprostone 143-147 tumor necrosis factor Homo sapiens 122-131 2507329-1 1989 The ability of interleukin-1 (IL-1 alpha), IL-1 beta, tumour necrosis factor alpha (TNF alpha) and bradykinin to cause prostaglandin E2 (PGE2) release from human synovial cells was examined. Dinoprostone 119-135 tumor necrosis factor Homo sapiens 84-93 2507329-1 1989 The ability of interleukin-1 (IL-1 alpha), IL-1 beta, tumour necrosis factor alpha (TNF alpha) and bradykinin to cause prostaglandin E2 (PGE2) release from human synovial cells was examined. Dinoprostone 137-141 tumor necrosis factor Homo sapiens 84-93 2507329-3 1989 When the cells were pretreated with IL-1 alpha or IL-1 beta for 24 h, their ability to release PGE2 in response to a short incubation (1 h) with bradykinin, TNF alpha or a second dose of IL-1 was potentiated. Dinoprostone 95-99 tumor necrosis factor Homo sapiens 157-166 2507329-7 1989 It seems likely, therefore, that activation of phospholipase A2 which occurs during a short incubation with IL-1, TNF alpha or bradykinin releases substrate, AA, which is more rapidly converted to PGE2 by cells in which CO has been induced. Dinoprostone 197-201 tumor necrosis factor Homo sapiens 114-123 2483117-3 1989 In this study, we present data demonstrating that alveolar macrophages (AMO) and peripheral blood monocytes (PBM) obtained from 10 normal volunteers display a significant difference in both the production of TNF and their susceptibility to TNF regulation by prostaglandin E2 (PGE2) and dexamethasone (Dex). Dinoprostone 258-274 tumor necrosis factor Homo sapiens 240-243 2483117-3 1989 In this study, we present data demonstrating that alveolar macrophages (AMO) and peripheral blood monocytes (PBM) obtained from 10 normal volunteers display a significant difference in both the production of TNF and their susceptibility to TNF regulation by prostaglandin E2 (PGE2) and dexamethasone (Dex). Dinoprostone 276-280 tumor necrosis factor Homo sapiens 208-211 2483117-3 1989 In this study, we present data demonstrating that alveolar macrophages (AMO) and peripheral blood monocytes (PBM) obtained from 10 normal volunteers display a significant difference in both the production of TNF and their susceptibility to TNF regulation by prostaglandin E2 (PGE2) and dexamethasone (Dex). Dinoprostone 276-280 tumor necrosis factor Homo sapiens 240-243 2483117-6 1989 PGE2 and Dex treatment of PBM suppressed LPS-induced TNF production by 78% and 72%, respectively, while AMO-TNF production was suppressed by only 22% and 33%. Dinoprostone 0-4 tumor necrosis factor Homo sapiens 53-56 2483117-7 1989 The accumulation of TNF mRNA in PBM was reduced 63% by PGE2 and 45% by Dex, as assessed by laser densitometry. Dinoprostone 55-59 tumor necrosis factor Homo sapiens 20-23 2483117-8 1989 Similar studies demonstrated that TNF mRNA accumulation in AMO was reduced 12% and 13% by PGE2 and Dex, respectively. Dinoprostone 90-94 tumor necrosis factor Homo sapiens 34-37 2723432-2 1989 PGE2, an immune mediator, is an inhibitor of LPS-stimulated TNF production and gene transcription. Dinoprostone 0-4 tumor necrosis factor Homo sapiens 60-63 2723432-3 1989 In the present study we determined whether pretreatment with PGE2 could desensitize the suppressive function of PGE2 for the production of macrophage (MO)-derived TNF. Dinoprostone 61-65 tumor necrosis factor Homo sapiens 163-166 2723432-3 1989 In the present study we determined whether pretreatment with PGE2 could desensitize the suppressive function of PGE2 for the production of macrophage (MO)-derived TNF. Dinoprostone 112-116 tumor necrosis factor Homo sapiens 163-166 2723432-5 1989 The concomitant addition of PGE2 with LPS shifted the LPS concentration-effect curve 16-fold to the right with a 52% decrease in the maximum LPS response, while MO pretreated with PGE2, washed, and incubated with LPS plus new PGE2 were desensitized to TNF regulation. Dinoprostone 28-32 tumor necrosis factor Homo sapiens 252-255 2723432-6 1989 These latter conditions resulted in a complete loss of the ability of PGE2 to inhibit MO TNF production as demonstrated by no significant change in the EC50 of LPS. Dinoprostone 70-74 tumor necrosis factor Homo sapiens 89-92 2723432-8 1989 At the transcriptional level, pretreatment of MO with PGE2 attenuated the ability of new PGE2 to inhibit LPS-dependent TNF mRNA expression. Dinoprostone 54-58 tumor necrosis factor Homo sapiens 119-122 2723432-8 1989 At the transcriptional level, pretreatment of MO with PGE2 attenuated the ability of new PGE2 to inhibit LPS-dependent TNF mRNA expression. Dinoprostone 89-93 tumor necrosis factor Homo sapiens 119-122 2723432-10 1989 MO pretreated with indomethacin also demonstrated an increased sensitivity for exogenous PGE2-induced suppression of TNF mRNA and bioactivity. Dinoprostone 89-93 tumor necrosis factor Homo sapiens 117-120 2506272-1 1989 Both IL-1 alpha and IL-1 beta and TNF-alpha induced a time- and dose-dependent release of authentic PGE2 from cultured human glomerular mesangial cells (HMC). Dinoprostone 100-104 tumor necrosis factor Homo sapiens 34-43 2506272-3 1989 Combinations of IL-1 and TNF-alpha when added simultaneously to HMC resulted in a dose-dependent synergistic increase in PGE2 production. Dinoprostone 121-125 tumor necrosis factor Homo sapiens 25-34 2473844-1 1989 The biological effects of tumor necrosis factor (TNF) include the enhancement of fibroblast proliferation, the secretion of collagenase and prostaglandin E2 (PGE2) by fibroblasts, and the resorption of bone and cartilage, suggesting a role for this cytokine in arthritic conditions. Dinoprostone 140-156 tumor necrosis factor Homo sapiens 26-47 2473844-1 1989 The biological effects of tumor necrosis factor (TNF) include the enhancement of fibroblast proliferation, the secretion of collagenase and prostaglandin E2 (PGE2) by fibroblasts, and the resorption of bone and cartilage, suggesting a role for this cytokine in arthritic conditions. Dinoprostone 140-156 tumor necrosis factor Homo sapiens 49-52 2473844-1 1989 The biological effects of tumor necrosis factor (TNF) include the enhancement of fibroblast proliferation, the secretion of collagenase and prostaglandin E2 (PGE2) by fibroblasts, and the resorption of bone and cartilage, suggesting a role for this cytokine in arthritic conditions. Dinoprostone 158-162 tumor necrosis factor Homo sapiens 26-47 2473844-1 1989 The biological effects of tumor necrosis factor (TNF) include the enhancement of fibroblast proliferation, the secretion of collagenase and prostaglandin E2 (PGE2) by fibroblasts, and the resorption of bone and cartilage, suggesting a role for this cytokine in arthritic conditions. Dinoprostone 158-162 tumor necrosis factor Homo sapiens 49-52 2507329-0 1989 Interleukin-1 potentiates bradykinin- and TNF alpha-induced PGE2 release. Dinoprostone 60-64 tumor necrosis factor Homo sapiens 42-51 2545692-5 1989 Besides inhibiting TNF alpha-induced cytotoxicity in L929 cells in the presence of actinomycin D, the TNF alpha INH impeded in a dose-dependent manner prostaglandin E2 production and expression of cell-associated interleukin-1 by human dermal fibroblasts. Dinoprostone 151-167 tumor necrosis factor Homo sapiens 102-111 2788408-5 1989 The increased production of prostaglandin E2, which is initiated when IL1 or TNF bind to the chondrocytes, was the same in the presence or absence of IGF 1. Dinoprostone 28-44 tumor necrosis factor Homo sapiens 77-80 2495247-6 1989 The TNF alpha and IL-1 activities induced by LPS and by LPS with IFN-gamma were reduced by PGE2, and stimulated by indomethacin. Dinoprostone 91-95 tumor necrosis factor Homo sapiens 4-13 2495247-0 1989 Control by IFN-gamma and PGE2 of TNF alpha and IL-1 production by human monocytes. Dinoprostone 25-29 tumor necrosis factor Homo sapiens 33-42 2548432-4 1989 PGE2 changed the dissociation constant of TNF for its receptors on U-937 cells only marginally, but it approximately doubled the number of binding sites. Dinoprostone 0-4 tumor necrosis factor Homo sapiens 42-45 2494431-9 1989 In contrast, the cyclooxygenase metabolite prostaglandin E2 inhibited the induction of TNF transcripts by TPA. Dinoprostone 43-59 tumor necrosis factor Homo sapiens 87-90 2913048-5 1989 In amnion cells in monolayer culture, TNF-alpha stimulated PGE2 formation, and TNF-alpha was cytostatic (inhibited [3H]thymidine incorporation into DNA) but not cytolytic in amnion cells. Dinoprostone 59-63 tumor necrosis factor Homo sapiens 38-47 2783319-8 1989 TNF-alpha also activated other SMC functions including the concentration-dependent release of PGE2 from SMC, and time-dependent induction of the gene for (2"-5")-oligoadenylate synthetase, an enzyme thought to mediate the anti-viral and anti-proliferative actions of IFN. Dinoprostone 94-98 tumor necrosis factor Homo sapiens 0-9 2784408-4 1989 In addition, IL-1 beta and TNF alpha were potent inducers of PGE2 production while exogenous PGE2 was growth inhibiting. Dinoprostone 61-65 tumor necrosis factor Homo sapiens 27-36 2784408-6 1989 Further examination of IL-1 beta- and TNF alpha-induced PGE2 secretion revealed IL-1 beta to be a more potent stimulator; however, this observation may be due, in part, to differences in the kinetics of induction. Dinoprostone 56-60 tumor necrosis factor Homo sapiens 38-47 2784408-7 1989 Rabbit anti-IL-1 beta and anti-TNF alpha specifically neutralized both proliferation and PGE2 production induced by these monokines, but anti-IL-1 beta (or anti-IL-1 alpha) did not block TNF alpha activity. Dinoprostone 89-93 tumor necrosis factor Homo sapiens 31-40 2783532-4 1989 Injection of endotoxin (2 mg/kg ip), human recombinant tumor necrosis factor-alpha (TNF alpha; 5 micrograms icv) or prostaglandin E2 (PGE2; 100 ng icv) all stimulated body temperature (0.9-1.6 degrees C) and Vo2 (18-25%); TNF alpha did not affect white blood cell count but increased BAT activity by 38%. Dinoprostone 116-132 tumor necrosis factor Homo sapiens 222-231 2674374-0 1989 Expression of IL-1 and tumor necrosis factor by endothelial cells: role in stimulating fibroblast PGE2 synthesis. Dinoprostone 98-102 tumor necrosis factor Homo sapiens 23-44 2674374-7 1989 Thus, elaboration of TNF by endothelial cells may allow detection of IL-1 in fibroblast PGE2 assays when the concentration of IL-1 is inadequate to stimulate thymocyte proliferation. Dinoprostone 88-92 tumor necrosis factor Homo sapiens 21-24 2494431-10 1989 Taken together, these results suggest that TPA induces TNF gene expression through the arachidonic acid cascade and that the level of TNF transcripts is regulated by metabolites of the pathway, leukotriene B4 and prostaglandin E2. Dinoprostone 213-229 tumor necrosis factor Homo sapiens 134-137 3165348-2 1988 Concomitant increase of prostaglandin E2 release was observed as a result of TNF-induced cell activation. Dinoprostone 24-40 tumor necrosis factor Homo sapiens 77-80 3293993-7 1988 The possibility was investigated that growth factors and TNF enhanced enzymatic conversion of PGI2 to 6k-PGE1, which stimulates bone resorption in mouse calvariae with a potency about one fourth that of PGE2. Dinoprostone 203-207 tumor necrosis factor Homo sapiens 57-60 3293993-10 1988 We conclude, on the basis of these new results and previously published data, that the cyclooxygenase product that acts as the mediator of bone resorption enhanced by growth factors and TNF in mouse calvariae is probably PGE2. Dinoprostone 221-225 tumor necrosis factor Homo sapiens 186-189 2838550-5 1988 Taken together, the experiments indicate that the TNF-induced production of PGE2 and the PGE2-induced increase of the intracellular cAMP concentration are essential elements of an auto-regulatory loop that controls the magnitude of the TNF-mediated effect in the macrophage. Dinoprostone 76-80 tumor necrosis factor Homo sapiens 50-53 2838550-5 1988 Taken together, the experiments indicate that the TNF-induced production of PGE2 and the PGE2-induced increase of the intracellular cAMP concentration are essential elements of an auto-regulatory loop that controls the magnitude of the TNF-mediated effect in the macrophage. Dinoprostone 76-80 tumor necrosis factor Homo sapiens 236-239 2838550-0 1988 Tumor necrosis factor-induced activation of peritoneal macrophages is regulated by prostaglandin E2 and cAMP. Dinoprostone 83-99 tumor necrosis factor Homo sapiens 0-21 2838550-5 1988 Taken together, the experiments indicate that the TNF-induced production of PGE2 and the PGE2-induced increase of the intracellular cAMP concentration are essential elements of an auto-regulatory loop that controls the magnitude of the TNF-mediated effect in the macrophage. Dinoprostone 89-93 tumor necrosis factor Homo sapiens 50-53 2838550-2 1988 This TNF-mediated effect is augmented by several substances that raise the intracellular concentration of cAMP, including PGE2, cholera toxin, and dibutyryl-cAMP. Dinoprostone 122-126 tumor necrosis factor Homo sapiens 5-8 2838550-3 1988 TNF also stimulates the endogenous production of PGE2 in cultures of peritoneal macrophages. Dinoprostone 49-53 tumor necrosis factor Homo sapiens 0-3 2838550-4 1988 The addition of the cyclo-oxygenase inhibitor, indomethacin, suppresses the TNF-mediated metabolic activation of macrophages, and this suppressive effect of indomethacin is overcome if exogenous PGE2 or cholera toxin is added to the culture. Dinoprostone 195-199 tumor necrosis factor Homo sapiens 76-79 2838550-5 1988 Taken together, the experiments indicate that the TNF-induced production of PGE2 and the PGE2-induced increase of the intracellular cAMP concentration are essential elements of an auto-regulatory loop that controls the magnitude of the TNF-mediated effect in the macrophage. Dinoprostone 89-93 tumor necrosis factor Homo sapiens 236-239 3131834-6 1988 These data show that tumor necrosis factor and interleukin-1 can both activate synovial cell PLA2 and induce generation of PGE2, but act in an additive rather than a synergistic fashion. Dinoprostone 123-127 tumor necrosis factor Homo sapiens 21-42 3260255-1 1988 TNF-alpha and IL-1 induce the production of PGE2 from human chondrosarcoma, fibrosarcoma, and carcinoma cell lines. Dinoprostone 44-48 tumor necrosis factor Homo sapiens 0-9 3260255-2 1988 When combined at sub-optimal concentrations, TNF-alpha and IL-1 synergistically stimulate PGE2 production. Dinoprostone 90-94 tumor necrosis factor Homo sapiens 45-54 3260255-3 1988 The synergy of TNF-alpha and IL-1 on the induction of PGE2 is partially neutralized by specific antibodies. Dinoprostone 54-58 tumor necrosis factor Homo sapiens 15-24 3131075-13 1987 Its production is also inhibited by glucocorticoids and prostaglandin E2, indicating that these substances play important roles in the regulation of TNF synthesis. Dinoprostone 56-72 tumor necrosis factor Homo sapiens 149-152 3266363-0 1988 Recombinant interleukin 1 and tumor necrosis factor acting in synergy to release thromboxane, 6-KETO-PGF1 alpha and PGE2 by human neutrophils. Dinoprostone 116-120 tumor necrosis factor Homo sapiens 30-51 3108890-4 1987 In 1 hr, TNF caused a sharp fall (2.5 degrees C) in body temperature and a large increase in plasma prostaglandin E2 levels. Dinoprostone 100-116 tumor necrosis factor Homo sapiens 9-12 3478137-12 1987 Although PGE2 (greater than 2 ng/ml) was able to suppress TNF production by monocytes, the addition of 10% plasma PGE2 was not enough to induce suppression. Dinoprostone 9-13 tumor necrosis factor Homo sapiens 58-61 3106013-5 1987 The magnitude of the PGE2 response, but not the calcium release, was less for bones treated with TNF than for those treated with equipotent doses of epidermal growth factor or human transforming growth factors-alpha or -beta, suggesting that the local site of production of PGE2 in bone may be different for TNF than for the other factors. Dinoprostone 21-25 tumor necrosis factor Homo sapiens 97-100 2999289-0 1985 Cachectin/tumor necrosis factor stimulates collagenase and prostaglandin E2 production by human synovial cells and dermal fibroblasts. Dinoprostone 59-75 tumor necrosis factor Homo sapiens 0-9 3490496-4 1986 In this report we demonstrate that epidermal growth factor and recombinant human transforming growth factor-alpha induce a significant rise in plasma calcium concentration when administered repeatedly to intact mice for periods ranging from 24 h to 16 d. The elevation of plasma calcium is not dependent on dietary calcium and is not invariably accompanied by an increase in systemic levels of the prostaglandin E2 metabolite 13,14-dihydro-15-keto-prostaglandin E2. Dinoprostone 398-414 tumor necrosis factor Homo sapiens 81-113 2999289-1 1985 Cachectin/TNF (tumor necrosis factor), an endotoxin-induced murine macrophage hormone implicated in the pathogenesis of cachexia and shock, has been found capable of stimulating collagenase and prostaglandin E2 (PGE2) production by isolated human synovial cells and dermal fibroblasts. Dinoprostone 194-210 tumor necrosis factor Homo sapiens 0-9 2999289-1 1985 Cachectin/TNF (tumor necrosis factor), an endotoxin-induced murine macrophage hormone implicated in the pathogenesis of cachexia and shock, has been found capable of stimulating collagenase and prostaglandin E2 (PGE2) production by isolated human synovial cells and dermal fibroblasts. Dinoprostone 194-210 tumor necrosis factor Homo sapiens 10-13 2999289-1 1985 Cachectin/TNF (tumor necrosis factor), an endotoxin-induced murine macrophage hormone implicated in the pathogenesis of cachexia and shock, has been found capable of stimulating collagenase and prostaglandin E2 (PGE2) production by isolated human synovial cells and dermal fibroblasts. Dinoprostone 212-216 tumor necrosis factor Homo sapiens 0-9 2999289-1 1985 Cachectin/TNF (tumor necrosis factor), an endotoxin-induced murine macrophage hormone implicated in the pathogenesis of cachexia and shock, has been found capable of stimulating collagenase and prostaglandin E2 (PGE2) production by isolated human synovial cells and dermal fibroblasts. Dinoprostone 212-216 tumor necrosis factor Homo sapiens 10-13 2999289-3 1985 The ability of cachectin/TNF to stimulate collagenase and PGE2 production suggests that it may play a role in tissue destruction and remodelling, as these processes occur in inflammatory diseases. Dinoprostone 58-62 tumor necrosis factor Homo sapiens 15-24 2999289-3 1985 The ability of cachectin/TNF to stimulate collagenase and PGE2 production suggests that it may play a role in tissue destruction and remodelling, as these processes occur in inflammatory diseases. Dinoprostone 58-62 tumor necrosis factor Homo sapiens 25-28 33478322-10 2021 Additionally, the physiomechanical properties of the encapsulating biomaterial have been shown to modulate clustering of TNF-alpha receptors on the encapsulated MSCs while regulating the production of anti-inflammatory factors such as indoleamine 2,3-dioxygenase (IDO) and prostaglandin E2 (PGE2) through activation of the P38 MAPK pathway. Dinoprostone 273-289 tumor necrosis factor Homo sapiens 121-130 33478322-10 2021 Additionally, the physiomechanical properties of the encapsulating biomaterial have been shown to modulate clustering of TNF-alpha receptors on the encapsulated MSCs while regulating the production of anti-inflammatory factors such as indoleamine 2,3-dioxygenase (IDO) and prostaglandin E2 (PGE2) through activation of the P38 MAPK pathway. Dinoprostone 291-295 tumor necrosis factor Homo sapiens 121-130 33573167-7 2021 Among them, 1,3-dihydroxy-2,8-dimethoxy-6-methylanthraquinone (1) suppressed the generation of ROS, NO, and PGE2 in tumor necrosis factor-alpha (TNF-alpha)-stimulated HDFs. Dinoprostone 108-112 tumor necrosis factor Homo sapiens 116-143 33796403-6 2021 In vitro experiments demonstrated that MF-766 restored PGE2-mediated inhibition of lipopolysaccharide (LPS)-induced tumor necrosis factor (TNF)-alpha production in THP-1 cells and human blood, and PGE2-mediated inhibition of interleukin (IL)-2-induced interferon (IFN)-gamma production in human NK cells. Dinoprostone 55-59 tumor necrosis factor Homo sapiens 116-149 32969101-3 2021 Our laboratory has previously shown that DSCs suppress Mphi TNFalpha production through secreted prostaglandin E2 . Dinoprostone 97-113 tumor necrosis factor Homo sapiens 60-68 32969101-13 2021 This suppression is distinct from the PGE2 -mediated Mphi TNFalpha suppression by DSC, suggesting that DSCs and CTBs regulate Mphi inflammation through distinct mechanisms. Dinoprostone 38-42 tumor necrosis factor Homo sapiens 58-66 33573167-7 2021 Among them, 1,3-dihydroxy-2,8-dimethoxy-6-methylanthraquinone (1) suppressed the generation of ROS, NO, and PGE2 in tumor necrosis factor-alpha (TNF-alpha)-stimulated HDFs. Dinoprostone 108-112 tumor necrosis factor Homo sapiens 145-154 33011237-10 2020 Single treatment of sPLA2-IIa, IL-1beta or TNF-alpha of HCjE cells induced minimal to no PGE2 production. Dinoprostone 89-93 tumor necrosis factor Homo sapiens 43-52 33553650-7 2021 Stimulation with IL-4 and TNF-alpha induced the generation of PGE2 in supernatants of conjunctival fibroblasts, and this production was significantly downregulated by ketotifen fumarate or steroids. Dinoprostone 62-66 tumor necrosis factor Homo sapiens 26-35 32990777-9 2020 RESULTS: TNFR2 and COX-2 were upregulated and the release of PGE2 was promoted by TNF-beta stimulation, which were all inhibited by Roflumilast. Dinoprostone 61-65 tumor necrosis factor Homo sapiens 82-90 33276479-5 2020 We found the merit of TMSCs as a therapeutic agent that retains favorable MSCs properties until relatively late passages and revealed that pre-treatment of TNF-alpha can enhance the immunomodulatory abilities of TMSCs through the upregulation of the PTGS2/PGE2 axis. Dinoprostone 256-260 tumor necrosis factor Homo sapiens 156-165 33011237-11 2020 When sPLA2-IIa was added to HCjE cells that were pre-treated with pro-inflammatory cytokines (TNF-alpha or IL-1beta), significant stimulation of PGE2 production was observed, concurrent with the extensive transcriptional changes of many inflammatory cytokines/chemokines and their receptors. Dinoprostone 145-149 tumor necrosis factor Homo sapiens 94-103 32927704-8 2020 The altered fatty acid profile was associated with an increased synthesis of the pro-inflammatory prostaglandin PGE2, which correlated with the upregulation of numerous NFkB-dependent pro-inflammatory mediators, including interleukin-1 (IL-1), interleukin-6 (IL-6), C-C motif chemokine ligand 2 (CCL2), and tumor necrosis factor-alpha (TNFalpha). Dinoprostone 112-116 tumor necrosis factor Homo sapiens 307-334 32978520-5 2020 COX2 is critical for the secretion of prostaglandin E2 and was strongly induced by H2O2 or TNFalpha only in presence of NRF2. Dinoprostone 38-54 tumor necrosis factor Homo sapiens 91-99 32927704-8 2020 The altered fatty acid profile was associated with an increased synthesis of the pro-inflammatory prostaglandin PGE2, which correlated with the upregulation of numerous NFkB-dependent pro-inflammatory mediators, including interleukin-1 (IL-1), interleukin-6 (IL-6), C-C motif chemokine ligand 2 (CCL2), and tumor necrosis factor-alpha (TNFalpha). Dinoprostone 112-116 tumor necrosis factor Homo sapiens 336-344 32265223-3 2020 Investigating these opposing activities, we found that tumor-derived prostaglandin E2 (PGE2) induces nuclear accumulation of p50 NF-kappaB in M-MDSCs, diverting their response to IFNgamma toward NO-mediated immunosuppression and reducing TNFalpha expression. Dinoprostone 69-85 tumor necrosis factor Homo sapiens 238-246 32323514-8 2020 In addition, MSCs increased PGE2 production after TNF-alpha/IFN-gamma stimulation, with the highest increase observed in MSC/SOCS1sh co-culture. Dinoprostone 28-32 tumor necrosis factor Homo sapiens 50-59 32765941-5 2020 Since PGE2, LXA4 and their precursors AA (arachidonic acid), dihomo-gamma-linolenic acid (DGLA) and gamma-linolenic acid (GLA) inhibit the production of pro-inflammatory IL-6 and TNF-alpha, they could be employed to treat cytokine storm seen in COVID-19, immune check point inhibitory (ICI) therapy, sepsis and ARDS (acute respiratory disease). Dinoprostone 6-10 tumor necrosis factor Homo sapiens 179-188 32265223-3 2020 Investigating these opposing activities, we found that tumor-derived prostaglandin E2 (PGE2) induces nuclear accumulation of p50 NF-kappaB in M-MDSCs, diverting their response to IFNgamma toward NO-mediated immunosuppression and reducing TNFalpha expression. Dinoprostone 87-91 tumor necrosis factor Homo sapiens 238-246 31120777-5 2020 IL-4 and TNF-alpha induced the generation of PGE2 and COX-2 in conjunctival and corneal cells. Dinoprostone 45-49 tumor necrosis factor Homo sapiens 9-18 33463295-4 2020 Lipopolysaccharide (LPS)-stimulated macrophages exhibited a dose-dependent decrease in gene expression and protein production of tumor necrosis factor alpha (TNF-alpha) when treated with PGE2. Dinoprostone 187-191 tumor necrosis factor Homo sapiens 129-156 33463295-4 2020 Lipopolysaccharide (LPS)-stimulated macrophages exhibited a dose-dependent decrease in gene expression and protein production of tumor necrosis factor alpha (TNF-alpha) when treated with PGE2. Dinoprostone 187-191 tumor necrosis factor Homo sapiens 158-167 32220961-7 2020 The TLR stimuli strongly induced miR-146a-5p, while PGE2 increased miR-99a-5p and miR-125a-5p, both implicated in down-regulation of TNFalpha. Dinoprostone 52-56 tumor necrosis factor Homo sapiens 133-141 32570711-6 2020 Activation of transforming growth factor-alpha-epidermal growth factor receptor (TGF-alpha-EGFR), nuclear factor kappa B (NF-kB), and cyclooxygenase 2- prostaglandin E2 (Cox2-PGE2) signaling all correlate with parathyroid cell proliferation, underlining their roles in the development of SHP. Dinoprostone 175-179 tumor necrosis factor Homo sapiens 14-46 31861245-7 2019 Compared with HD/ASCs, untreated and tumour necrosis factor (TNF) + interferon (IFN)-gamma (TI)-treated RD/ASCs produced similar amounts of prostaglandin E2 (PGE2), IL-6, leukemia inhibiting factor (LIF), and TGF-beta1, more IL-1Ra, soluble human leukocyte antigen G (sHLA-G) and tumor necrosis factor-inducible gene (TSG)-6, but less kynurenines and galectin-3. Dinoprostone 140-156 tumor necrosis factor Homo sapiens 61-64 31986892-12 2020 In conclusion, we found crosstalk between PGE2 and TNF-alpha signaling pathways, and the interaction between GRK2 and TRAF2 led to the activation of TNF-alpha-TRAF2-MMP-9 signaling and resulted in the progression of LSCC. Dinoprostone 42-46 tumor necrosis factor Homo sapiens 149-158 32014738-4 2020 RESULTS: Human amnion tissue explants treated with LPS, IL-1beta, or TNF-alpha increased production of prostaglandin E2 (PGE2; p < 0.05) but decreased PGFM. Dinoprostone 103-119 tumor necrosis factor Homo sapiens 69-78 32014738-4 2020 RESULTS: Human amnion tissue explants treated with LPS, IL-1beta, or TNF-alpha increased production of prostaglandin E2 (PGE2; p < 0.05) but decreased PGFM. Dinoprostone 121-125 tumor necrosis factor Homo sapiens 69-78 30415531-5 2019 However, TNF-alpha production which was inhibited by PGE-2+LPS increased by pLTA treatment. Dinoprostone 53-58 tumor necrosis factor Homo sapiens 9-18 31008484-5 2019 The results showed that, PGE2 increased interleukin 6 (IL-6) and tumor necrosis factor alpha (TNFalpha) output, decreased chemokine (c-x-c motif) ligand 8 (CXCL8) output in a dose-dependent manner, but had no effect on IL-1beta and chemokine (c-c motif) ligand 2 (CCL-2) secretion of HUSMCs. Dinoprostone 25-29 tumor necrosis factor Homo sapiens 65-92 31008484-5 2019 The results showed that, PGE2 increased interleukin 6 (IL-6) and tumor necrosis factor alpha (TNFalpha) output, decreased chemokine (c-x-c motif) ligand 8 (CXCL8) output in a dose-dependent manner, but had no effect on IL-1beta and chemokine (c-c motif) ligand 2 (CCL-2) secretion of HUSMCs. Dinoprostone 25-29 tumor necrosis factor Homo sapiens 94-102 31048000-13 2019 In addition, IL-6, IL-8, and TNF-alpha formation were also inhibited, but sometimes independently of PGE2. Dinoprostone 101-105 tumor necrosis factor Homo sapiens 29-38 30415531-6 2019 The regulatory effects of IL-10 and TNF-alpha induced by PGE-2 and LPS in PMA-differentiated THP-1 cells were mediated by pLTA, but not by other LTAs isolated from either Staphylococcus aureus (aLTA) or L. sakei (sLTA). Dinoprostone 57-62 tumor necrosis factor Homo sapiens 36-45 30415531-7 2019 Further studies revealed that pLTA-mediated IL-10 inhibition and TNF-alpha induction in PGE-2+LPS-stimulated PMA-differentiated THP-1 cells were mediated by dephosphorylation of p38 and phosphorylation of c-Jun N-terminal kinase (JNK), respectively. Dinoprostone 88-93 tumor necrosis factor Homo sapiens 65-74 30190207-6 2018 INTERPRETATION: Our work indicates that COX-2-PGE2 signaling could be a novel target for the management of PNRs to TNF inhibitors. Dinoprostone 46-50 tumor necrosis factor Homo sapiens 115-118 29796776-11 2018 Lastly, we observed that DHA not only reduced the PGE2 levels in tumor necrosis factor-alpha (TNF-alpha)-treated ECs but also blunted the upregulation of inflammatory cytokines of interleukin (IL)-6 and IL-1beta induced by TNF-alpha or PGE2. Dinoprostone 50-54 tumor necrosis factor Homo sapiens 65-92 29796776-11 2018 Lastly, we observed that DHA not only reduced the PGE2 levels in tumor necrosis factor-alpha (TNF-alpha)-treated ECs but also blunted the upregulation of inflammatory cytokines of interleukin (IL)-6 and IL-1beta induced by TNF-alpha or PGE2. Dinoprostone 50-54 tumor necrosis factor Homo sapiens 94-103 29796776-11 2018 Lastly, we observed that DHA not only reduced the PGE2 levels in tumor necrosis factor-alpha (TNF-alpha)-treated ECs but also blunted the upregulation of inflammatory cytokines of interleukin (IL)-6 and IL-1beta induced by TNF-alpha or PGE2. Dinoprostone 236-240 tumor necrosis factor Homo sapiens 94-103 29929938-0 2019 PGE2 enhanced TNFalpha-mediated IL-8 induction in monocytic cell lines and PBMC. Dinoprostone 0-4 tumor necrosis factor Homo sapiens 14-22 29929938-4 2019 KEY RESULTS: In monocytic cell lines THP-1, MonoMac and U937 PGE2 had only a marginal impact on IL-8 induction but strongly enhanced TNFalpha-induced IL-8 mRNA and protein synthesis. Dinoprostone 61-65 tumor necrosis factor Homo sapiens 133-141 29929938-7 2019 Stimulation of THP-1 cells with an EP4 specific agonist enhanced TNFalpha-induced IL-8 mRNA and protein formation to the same extent as PGE2. Dinoprostone 136-140 tumor necrosis factor Homo sapiens 65-73 29929938-8 2019 In HEK293 cells expressing EP4, but not in wild type HEK293 cells lacking EP4, PGE2 enhanced TNFalpha-induced IL-8 protein and mRNA synthesis. Dinoprostone 79-83 tumor necrosis factor Homo sapiens 93-101 29929938-9 2019 In THP-1 cells, the enhancement of TNFalpha-mediated IL-8 mRNA induction by PGE2 was mimicked by a PKA-activator. Dinoprostone 76-80 tumor necrosis factor Homo sapiens 35-43 29929938-10 2019 Furthermore in these cells PGE2 induced expression of transcription factor C/EBPss, enhanced NF-kappaB activation by TNFalpha and inhibited TNFalpha-mediated AP-1 activation. Dinoprostone 27-31 tumor necrosis factor Homo sapiens 117-125 29929938-10 2019 Furthermore in these cells PGE2 induced expression of transcription factor C/EBPss, enhanced NF-kappaB activation by TNFalpha and inhibited TNFalpha-mediated AP-1 activation. Dinoprostone 27-31 tumor necrosis factor Homo sapiens 140-148 30053598-9 2018 PGE2 and also EP2 and EP4 agonists (but not EP1 or EP3 agonists) suppressed TNF-alpha production in blood and THP-1 cells. Dinoprostone 0-4 tumor necrosis factor Homo sapiens 76-85 30053598-12 2018 This indicates that PGE2 suppression of TNF-alpha by human monocytic cells occurs via EP2R and EP4R expression. Dinoprostone 20-24 tumor necrosis factor Homo sapiens 40-49 28659609-6 2017 The same feedback mechanism contributes to PGE2-mediated suppression of TNF release. Dinoprostone 43-47 tumor necrosis factor Homo sapiens 72-75 29848388-9 2018 Having reported in 1985 that TNF/cachectin also induced collagenase and PGE2 in human synovial cells, we found that IL-1Ra did not block TNF-alpha but was due to another inhibitor. Dinoprostone 72-76 tumor necrosis factor Homo sapiens 29-32 29848388-9 2018 Having reported in 1985 that TNF/cachectin also induced collagenase and PGE2 in human synovial cells, we found that IL-1Ra did not block TNF-alpha but was due to another inhibitor. Dinoprostone 72-76 tumor necrosis factor Homo sapiens 33-42 29272001-13 2017 After the intervention of PGE2 and Butaprost, great increases were seen in the cell proliferation rate, invasion capability, and the expression of MMP-9, VEGF, IL-6, and TNF-alpha in EC109 and TE-1 cell strains (p < 0.05), however, the intervention of RNAi could reduce above indexes (p < 0.05). Dinoprostone 26-30 tumor necrosis factor Homo sapiens 170-179 30486522-3 2018 The mechanism is mainly by inhibiting the activation of nuclear factor (NF-kappaB), mitogen-activated protein kinase (MAPKs) and signal transducers and activators of transcription (STAT) signaling pathways and down-regulating the inflammatory gene expression including tumor necrosis factor-alpha (TNF-alpha), prostaglandin E2 (PGE2), nitric oxide (NO), interleukin-1(IL-1), IL-6, IL-8 and other inflammatory factors. Dinoprostone 310-326 tumor necrosis factor Homo sapiens 298-307 30486522-3 2018 The mechanism is mainly by inhibiting the activation of nuclear factor (NF-kappaB), mitogen-activated protein kinase (MAPKs) and signal transducers and activators of transcription (STAT) signaling pathways and down-regulating the inflammatory gene expression including tumor necrosis factor-alpha (TNF-alpha), prostaglandin E2 (PGE2), nitric oxide (NO), interleukin-1(IL-1), IL-6, IL-8 and other inflammatory factors. Dinoprostone 328-332 tumor necrosis factor Homo sapiens 298-307 27932980-3 2016 We found that TNF-alpha-stimulated increases in cPLA2 mRNA (5.2 folds) and protein (3.9 folds) expression, promoter activity (4.3 folds), and PGE2 secretion (4.7 folds) in HPAEpiCs, determined by Western blot, real-time PCR, promoter activity assay and PGE2 ELISA kit. Dinoprostone 142-146 tumor necrosis factor Homo sapiens 14-23 29682085-9 2017 The early, constitutive presence of PGE2 significantly reduced astrocyte-produced TNF-alpha, while delayed administration had no effect. Dinoprostone 36-40 tumor necrosis factor Homo sapiens 82-91 28181858-9 2017 TNFalpha stimulation increased expression of IL-6 at both RNA and protein level as well as upregulated COX2 gene expression and PTGES1.Stimulation with both INFgamma and TNFalpha resulted in significant increase in PGE2 levels in cell culture medium. Dinoprostone 215-219 tumor necrosis factor Homo sapiens 0-8 28181858-9 2017 TNFalpha stimulation increased expression of IL-6 at both RNA and protein level as well as upregulated COX2 gene expression and PTGES1.Stimulation with both INFgamma and TNFalpha resulted in significant increase in PGE2 levels in cell culture medium. Dinoprostone 215-219 tumor necrosis factor Homo sapiens 170-178 28284832-4 2017 Furthermore, the bioactivity lasted at least 28days, demonstrated by a 80-95% inhibition of PGE2 production using TNFalpha-stimulated chondrocyte culture, indicating inhibition of inflammation. Dinoprostone 92-96 tumor necrosis factor Homo sapiens 114-122 28298525-13 2017 Furthermore, fever might therefore occur in the absence of a septic shock response because of the inhibiting effect of PGE2 on TNF-alpha production. Dinoprostone 119-123 tumor necrosis factor Homo sapiens 127-136 27658124-9 2017 TNF-alpha significantly increased (P < 0.05) PGE-2 but had no effect on PGF-2alpha secretion or on the PGF-2alpha:PGE2 ratio. Dinoprostone 48-53 tumor necrosis factor Homo sapiens 0-9 28400287-11 2017 RESULTS: In irradiated or TNF-alpha stimulated HaCaT cells the formation of IL-6 and PGE2 or NF-kappaB activation was strongly reduced by PE. Dinoprostone 85-89 tumor necrosis factor Homo sapiens 26-35 28410380-9 2017 Unlike IL-10, PGE2 is absent from peritoneal fluid of patients with benign conditions and selectively reduces TNFalpha induction in response to TLR-mediated activation in the presence of OC-associated ascites. Dinoprostone 14-18 tumor necrosis factor Homo sapiens 110-118 27658702-6 2017 RESULTS: TNFalpha dose-dependently increased NO, PGE2 and MMP activity (all p < 0.001) and induced MMP-13 (p < 0.05) and ADAMTS-5 gene expression (pp < 0.01) with values greater at 5 % oxygen tension than 21 %. Dinoprostone 49-53 tumor necrosis factor Homo sapiens 9-17 27658702-9 2017 CONCLUSIONS: The present findings revealed that TNFalpha increased production of NO, PGE2 and MMP activity at 5 % oxygen tension. Dinoprostone 85-89 tumor necrosis factor Homo sapiens 48-56 28592915-3 2017 Analyzing cocultures of platelets and murine bone marrow-derived macrophages or human monocytes, we found that collagen-activated platelets release high amounts of prostaglandin E2 (PGE2) that leads to an increased interleukin- (IL-) 10 release and a decreased tumor necrosis factor (TNF) alpha secretion out of the monocytes or macrophages. Dinoprostone 164-180 tumor necrosis factor Homo sapiens 261-294 28592915-3 2017 Analyzing cocultures of platelets and murine bone marrow-derived macrophages or human monocytes, we found that collagen-activated platelets release high amounts of prostaglandin E2 (PGE2) that leads to an increased interleukin- (IL-) 10 release and a decreased tumor necrosis factor (TNF) alpha secretion out of the monocytes or macrophages. Dinoprostone 182-186 tumor necrosis factor Homo sapiens 261-294 27932980-3 2016 We found that TNF-alpha-stimulated increases in cPLA2 mRNA (5.2 folds) and protein (3.9 folds) expression, promoter activity (4.3 folds), and PGE2 secretion (4.7 folds) in HPAEpiCs, determined by Western blot, real-time PCR, promoter activity assay and PGE2 ELISA kit. Dinoprostone 253-257 tumor necrosis factor Homo sapiens 14-23 28955943-9 2016 Downstream of COX2, the levels of PGE2 were increased only in TNFalpha-stimulated, LMWF-5A-treated cells; however, in both IL-1beta- and TNFalpha-stimulated cells, LMWF-5A increased the release of the anti-inflammatory prostaglandin PGD2. Dinoprostone 34-38 tumor necrosis factor Homo sapiens 62-70 27460634-11 2016 EP2 receptor-selective antagonists had marginal effects on the PGE2 inhibition of TNF-alpha generation, whereas EP4 receptor-selective antagonists caused rightward shifts in the PGE2 concentration-response curves. Dinoprostone 63-67 tumor necrosis factor Homo sapiens 82-91 26817996-2 2016 Unexpectedly, we observed that the critical soluble mediators of type-1 immune effector cells, IFNgamma and TNFalpha, synergize in the induction of cyclooxygenase 2 (COX2), the key enzyme in prostaglandin (PG)E2 synthesis, and the subsequent hyperactivation of myeloid-derived suppressor cells (MDSC) within the tumor microenvironment (TME) of ovarian cancer patients. Dinoprostone 191-211 tumor necrosis factor Homo sapiens 108-116 27020304-2 2016 Compound 4f showed an IC50 of 123nM for inhibition of PGE2-induced TNFalpha reduction in an ex vivo LPS-stimulated human whole blood assay (showing >10-fold increase over clinical compound CJ-023,423). Dinoprostone 54-58 tumor necrosis factor Homo sapiens 67-75 27097228-5 2016 A decreased expression pattern of induced COX-2 and reduced production of downstream PGE2 occurred upon TNF-alpha stimulation in G6PD-kd A549 cells compared with scramble control A549 cells. Dinoprostone 85-89 tumor necrosis factor Homo sapiens 104-113 26912133-10 2016 After 24-months of TNF blockade, IL-23 and PGE2 remained elevated with higher levels compared with the healthy group (p < 0.001 and p = 0.03) in spite of significant improvements in all clinical/inflammatory parameters (p < 0.001). Dinoprostone 43-47 tumor necrosis factor Homo sapiens 19-22 26447753-7 2016 Serum levels of PGE2 were positively correlated with probing depth (PD) and clinical attachment level (CAL) as well as with GCF levels of TNF-alpha in women with PTB. Dinoprostone 16-20 tumor necrosis factor Homo sapiens 138-147 26590114-7 2015 Fisetin also inhibited the production of NO, PGE2 IL-1beta, IL-6, expression of iNOS and COX-2, and activation of NF-kappaB in HaCaT cells treated with TNF-alpha. Dinoprostone 45-49 tumor necrosis factor Homo sapiens 152-161 26098693-6 2016 In combination with another proinflammatory mediator found elevated in asthmatic airways, the cytokine TNF-alpha, we observed that S1P-induced COX-2 mRNA expression and protein up-regulation and PGE2 secretion from ASM cells were significantly enhanced. Dinoprostone 195-199 tumor necrosis factor Homo sapiens 103-112 26415983-5 2015 The results showed that both PGE2 and TNF-alpha up-regulated the expressions of CD40, CD80, CD83, CD86, and MHC-II, decreased the antigen uptake of DCs, and DCs stimulated by PGE2 or TNF-alpha could increase T cell proliferation. Dinoprostone 29-33 tumor necrosis factor Homo sapiens 183-192 26415983-5 2015 The results showed that both PGE2 and TNF-alpha up-regulated the expressions of CD40, CD80, CD83, CD86, and MHC-II, decreased the antigen uptake of DCs, and DCs stimulated by PGE2 or TNF-alpha could increase T cell proliferation. Dinoprostone 175-179 tumor necrosis factor Homo sapiens 38-47 26415983-11 2015 These results demonstrate that PGE2 and TNF-alpha could enhance DCs functions by mediating PGE2-EP4-cAMP pathway, TNF-alpha-TNFR1-TRADD-TRAF2-NF-kappaB pathway respectively. Dinoprostone 31-35 tumor necrosis factor Homo sapiens 114-123 26415983-11 2015 These results demonstrate that PGE2 and TNF-alpha could enhance DCs functions by mediating PGE2-EP4-cAMP pathway, TNF-alpha-TNFR1-TRADD-TRAF2-NF-kappaB pathway respectively. Dinoprostone 91-95 tumor necrosis factor Homo sapiens 40-49 26634864-9 2016 TNF-alpha induced PGE2 release was reduced in presence of naproxen sodium (p < 0.05), in association with decreased COX-2 and increased HPDG mRNAs expression. Dinoprostone 18-22 tumor necrosis factor Homo sapiens 0-9 26123748-0 2015 Response to tumor necrosis factor-alpha mediated inflammation involving activation of prostaglandin E2 and Wnt signaling in nucleus pulposus cells. Dinoprostone 86-102 tumor necrosis factor Homo sapiens 12-39 26123748-2 2015 However, it is not known whether crosstalk between tumor necrosis factor-alpha(TNF-alpha)-PGE2 -mediated signaling and Wnt signaling plays a role in the regulation of intervertebral disc (IVD) cells. Dinoprostone 90-94 tumor necrosis factor Homo sapiens 51-78 26123748-2 2015 However, it is not known whether crosstalk between tumor necrosis factor-alpha(TNF-alpha)-PGE2 -mediated signaling and Wnt signaling plays a role in the regulation of intervertebral disc (IVD) cells. Dinoprostone 90-94 tumor necrosis factor Homo sapiens 79-88 26123748-3 2015 In this study, we investigated the relationship between TNF-alpha-PGE2 signaling and Wnt signaling in IVD cells. Dinoprostone 66-70 tumor necrosis factor Homo sapiens 56-65 26210574-8 2015 Additionally, there was a strong correlation between increased prostaglandin E2 (PGE2) and reduction of TNF-alpha. Dinoprostone 63-79 tumor necrosis factor Homo sapiens 104-113 26123748-5 2015 The EP receptors EP1, EP3, and EP4 were expressed in IVD cells, and TNF-alpha significantly increased PGE2 production. Dinoprostone 102-106 tumor necrosis factor Homo sapiens 68-77 26123748-9 2015 We conclude that TNF-alpha-induced COX-2 and PGE2 stimulate Wnt signaling and activate Wnt target genes. Dinoprostone 45-49 tumor necrosis factor Homo sapiens 17-26 26123748-10 2015 Suppression of the EP3 receptor via TNF-alpha-PGE2 signaling seems to suppress IVD degeneration by controlling the activation of Wnt signaling. Dinoprostone 46-50 tumor necrosis factor Homo sapiens 36-45 26210574-8 2015 Additionally, there was a strong correlation between increased prostaglandin E2 (PGE2) and reduction of TNF-alpha. Dinoprostone 81-85 tumor necrosis factor Homo sapiens 104-113 25958832-9 2015 MLR and covariate analysis revealed that macrophage TNF-alpha was strongly dependent on the MSC activation factor, PGE2 level, and macrophage donor but not MSC culture format (monolayer versus encapsulated). Dinoprostone 115-119 tumor necrosis factor Homo sapiens 52-61 25865800-4 2015 Activation of human MoDC resulted in the release of TNFalpha and IL-1beta that in turn stimulated MMP-1 (human collagenase) and PGE2 secretion by human dermal fibroblasts. Dinoprostone 128-132 tumor necrosis factor Homo sapiens 52-60 25866079-0 2015 The hydroxytyrosol-dependent increase of TNF-alpha in LPS-activated human monocytes is mediated by PGE2 and adenylate cyclase activation. Dinoprostone 99-103 tumor necrosis factor Homo sapiens 41-50 25866079-5 2015 Exogenous PGE2 reduced both TNF-alpha mRNA and TNF-alpha secretion (EIA assay) while the activation of adenylate cyclase by forskolin decreased only the TNF-alpha secretion but did not influence the TNF-alpha mRNA level. Dinoprostone 10-14 tumor necrosis factor Homo sapiens 28-37 25866079-5 2015 Exogenous PGE2 reduced both TNF-alpha mRNA and TNF-alpha secretion (EIA assay) while the activation of adenylate cyclase by forskolin decreased only the TNF-alpha secretion but did not influence the TNF-alpha mRNA level. Dinoprostone 10-14 tumor necrosis factor Homo sapiens 47-56 25866079-5 2015 Exogenous PGE2 reduced both TNF-alpha mRNA and TNF-alpha secretion (EIA assay) while the activation of adenylate cyclase by forskolin decreased only the TNF-alpha secretion but did not influence the TNF-alpha mRNA level. Dinoprostone 10-14 tumor necrosis factor Homo sapiens 47-56 25866079-5 2015 Exogenous PGE2 reduced both TNF-alpha mRNA and TNF-alpha secretion (EIA assay) while the activation of adenylate cyclase by forskolin decreased only the TNF-alpha secretion but did not influence the TNF-alpha mRNA level. Dinoprostone 10-14 tumor necrosis factor Homo sapiens 47-56 26091726-2 2015 Described herein is a class of amphoteric EP4 antagonists which reverses PGE2-induced suppression of TNFalpha production in human whole blood. Dinoprostone 73-77 tumor necrosis factor Homo sapiens 101-109 25218510-5 2015 Interestingly, genetic disruption of tnf-alpha, its receptors tnf-r1/r2, and cox-2 and pharmacological inhibition of COX-2 activity enhanced LPS-induced IL-10 production in microglia, which suggests negative regulation of IL-10 induction by the earlier-released TNF-alpha and PGE2. Dinoprostone 276-280 tumor necrosis factor Homo sapiens 37-46 25218510-6 2015 Further studies showed that negative regulation of IL-10 production by TNF-alpha is mediated by PGE2. Dinoprostone 96-100 tumor necrosis factor Homo sapiens 71-80 26000299-3 2015 To compare the effects of these treatments on chondrocyte metabolism, TNF-alpha was incubated with cultured chondrocytes to mimic a proinflammatory environment with increasing production of MMP-1 and prostaglandin E2 (PGE2). Dinoprostone 200-216 tumor necrosis factor Homo sapiens 70-79 25046208-9 2015 Knockdown of cIAP1 and cIAP2 in primary myometrial cells significantly decreased TNF-alpha induced expression and secretion of pro-inflammatory cytokines (IL-6 and IL-8); cyclooxygenase (COX)-2 expression and subsequent release of the prostaglandin PGE2 ; the expression and secretion of MMP-9; and NF-kappaB transcriptional activity. Dinoprostone 249-253 tumor necrosis factor Homo sapiens 81-90 25949900-3 2015 Co-culture with activated gammadelta T cells induced an upregulation of Cox-2 expression in Colo357 cells, and thereby an enhanced PGE2 release, in response to tumor necrosis factor alpha (TNFalpha) secretion from gammadelta T cells. Dinoprostone 131-135 tumor necrosis factor Homo sapiens 160-187 25949900-3 2015 Co-culture with activated gammadelta T cells induced an upregulation of Cox-2 expression in Colo357 cells, and thereby an enhanced PGE2 release, in response to tumor necrosis factor alpha (TNFalpha) secretion from gammadelta T cells. Dinoprostone 131-135 tumor necrosis factor Homo sapiens 189-197 25785838-0 2015 Stromal cells positively and negatively modulate the growth of cancer cells: stimulation via the PGE2-TNFalpha-IL-6 pathway and inhibition via secreted GAPDH-E-cadherin interaction. Dinoprostone 97-101 tumor necrosis factor Homo sapiens 102-110 25562426-0 2015 PKCdelta-iPLA2-PGE2-PPARgamma signaling cascade mediates TNF-alpha induced Claudin 1 expression in human lung carcinoma cells. Dinoprostone 15-19 tumor necrosis factor Homo sapiens 57-66 25562426-9 2015 In conclusion, TNF-alpha induced CLDN1 expression is regulated by the PKCdelta-iPLA2-PGE2-PPARgamma signaling cascade in human lung carcinoma A549 cells. Dinoprostone 85-89 tumor necrosis factor Homo sapiens 15-24 25163981-3 2015 Prostaglandin E2 (PGE2) production stimulated by TNFalpha was used as a parameter of inflammation. Dinoprostone 0-16 tumor necrosis factor Homo sapiens 49-57 25163981-3 2015 Prostaglandin E2 (PGE2) production stimulated by TNFalpha was used as a parameter of inflammation. Dinoprostone 18-22 tumor necrosis factor Homo sapiens 49-57 25163981-8 2015 In the bioactivity assay, PGE2 levels induced by TNFalpha were reduced to an average of 30% using microspheres loaded with 0.1 nmol CXB per transwell; with microspheres loaded with 0.1 nmol TA, PGE2 production was initially reduced to 3% and gradually recovered to 30% reduction. Dinoprostone 26-30 tumor necrosis factor Homo sapiens 49-57 25446010-7 2015 BRE inhibited TNF-alpha/IL-1beta-induced NFkappaB p65 nuclear translocation, PGE2 production, up-regulation of COX-2, ICAM-1 and VCAM-1 gene and protein expression and leukocyte binding in HEMEC but not in HIMEC. Dinoprostone 77-81 tumor necrosis factor Homo sapiens 14-23 25014275-6 2014 We observed that PGE2 decreased tumor necrosis factor-alpha (TNF-alpha) production evoked by poly(I:C), whereas PGE2 potentiated poly(I:C)-triggered interleukin-8 (IL-8) production. Dinoprostone 17-21 tumor necrosis factor Homo sapiens 61-70 26267111-6 2014 All affibody molecules could inhibit IL-6 and PGE2 production in TNF-alpha-stimulated MH7A cells. Dinoprostone 46-50 tumor necrosis factor Homo sapiens 65-74 25090227-7 2014 Among the anti-inflammatory cytokines, the production of prostaglandin E2 (PGE2) and the expression of its primary enzyme, cyclooxygenase-2 (COX-2), were profoundly increased by pre-stimulation with interferon gamma (IFN-gamma) and tumor necrosis factor alpha (TNF-alpha), and this response was significantly decreased with consecutive passages. Dinoprostone 57-73 tumor necrosis factor Homo sapiens 232-259 24120915-7 2014 The strong inflammatory property of TNFalpha was mirrored by its activation of COX-2 and inhibition of prostaglandin E2 (PGE2) catabolism. Dinoprostone 103-119 tumor necrosis factor Homo sapiens 36-44 24120915-7 2014 The strong inflammatory property of TNFalpha was mirrored by its activation of COX-2 and inhibition of prostaglandin E2 (PGE2) catabolism. Dinoprostone 121-125 tumor necrosis factor Homo sapiens 36-44 25090227-7 2014 Among the anti-inflammatory cytokines, the production of prostaglandin E2 (PGE2) and the expression of its primary enzyme, cyclooxygenase-2 (COX-2), were profoundly increased by pre-stimulation with interferon gamma (IFN-gamma) and tumor necrosis factor alpha (TNF-alpha), and this response was significantly decreased with consecutive passages. Dinoprostone 57-73 tumor necrosis factor Homo sapiens 261-270 24441870-3 2014 Here, we demonstrated that TNF-alpha induced cPLA2 mRNA and protein expression, promoter activity, and PGE2 secretion in HPAEpiCs. Dinoprostone 103-107 tumor necrosis factor Homo sapiens 27-36 24441870-11 2014 The activity of cPLA2 protein upregulated by TNF-alpha was reflected on the PGE2 release, which was reduced by AG490, AG1296, LY294002, or PD98059. Dinoprostone 76-80 tumor necrosis factor Homo sapiens 45-54 24055878-5 2014 LPS induced the production of TNF-alpha, but not IL-1beta An anti-TNF-alpha neutralizing Ab significantly inhibited PGE2 production and COX2 mRNA expression in response to LPS. Dinoprostone 117-121 tumor necrosis factor Homo sapiens 30-39 24055878-5 2014 LPS induced the production of TNF-alpha, but not IL-1beta An anti-TNF-alpha neutralizing Ab significantly inhibited PGE2 production and COX2 mRNA expression in response to LPS. Dinoprostone 117-121 tumor necrosis factor Homo sapiens 67-76 24226202-9 2014 Furthermore, both gene knockdown and pharmacological inhibition studies showed that COX-2 mediates the TNF-alpha/IL-8 pathway by increasing the production of prostaglandin E2 (PGE2). Dinoprostone 158-174 tumor necrosis factor Homo sapiens 103-112 24226202-9 2014 Furthermore, both gene knockdown and pharmacological inhibition studies showed that COX-2 mediates the TNF-alpha/IL-8 pathway by increasing the production of prostaglandin E2 (PGE2). Dinoprostone 176-180 tumor necrosis factor Homo sapiens 103-112 24441870-12 2014 Taken together, these results demonstrated that TNF-alpha-induced cPLA2 expression and PGE2 release were mediated through a Jak2/PDGFR/PI3K/Akt/p42/p44 MAPK/Elk-1 pathway in HPAEpiCs. Dinoprostone 87-91 tumor necrosis factor Homo sapiens 48-57 24189030-9 2014 RESULTS: PK exhibited a higher response to TNF-alpha than NHK regarding the ICAM-1 expression and the production of NO, IL-6, IL-8, fractalkine and PGE2, whereas BS-EAcf significantly inhibited this TNF-alpha-induced increase at concentrations without causing keratinocyte toxicity. Dinoprostone 148-152 tumor necrosis factor Homo sapiens 43-52 24349530-4 2013 METHODS: The involvement of cPLA2alpha in tumor necrosis factor (TNF)-induced intracellular signaling cascades in synoviocytes (synovial fibroblast-like cells) was analyzed by arachidonic acid (AA) release assay, synoviocyte enzyme activity assay, gene expression analysis by real-time PCR and ELISA immunoassay for the detection of prostaglandin E2 (PGE2), interleukin 8 (IL8) and stromelysin-1 (MMP3), respectively. Dinoprostone 351-355 tumor necrosis factor Homo sapiens 42-63 24344780-0 2013 LPS and TNF alpha modulate AMPA/NMDA receptor subunit expression and induce PGE2 and glutamate release in preterm fetal ovine mixed glial cultures. Dinoprostone 76-80 tumor necrosis factor Homo sapiens 8-17 24344780-7 2013 Furthermore, we demonstrate that glutamate and prostaglandin E2 (PGE2) release following TNF-alpha or LPS are mediated by a TNF-alpha-COX-2 dependent mechanism. Dinoprostone 47-63 tumor necrosis factor Homo sapiens 89-98 24344780-7 2013 Furthermore, we demonstrate that glutamate and prostaglandin E2 (PGE2) release following TNF-alpha or LPS are mediated by a TNF-alpha-COX-2 dependent mechanism. Dinoprostone 47-63 tumor necrosis factor Homo sapiens 124-133 24344780-7 2013 Furthermore, we demonstrate that glutamate and prostaglandin E2 (PGE2) release following TNF-alpha or LPS are mediated by a TNF-alpha-COX-2 dependent mechanism. Dinoprostone 65-69 tumor necrosis factor Homo sapiens 89-98 24344780-7 2013 Furthermore, we demonstrate that glutamate and prostaglandin E2 (PGE2) release following TNF-alpha or LPS are mediated by a TNF-alpha-COX-2 dependent mechanism. Dinoprostone 65-69 tumor necrosis factor Homo sapiens 124-133 24349530-4 2013 METHODS: The involvement of cPLA2alpha in tumor necrosis factor (TNF)-induced intracellular signaling cascades in synoviocytes (synovial fibroblast-like cells) was analyzed by arachidonic acid (AA) release assay, synoviocyte enzyme activity assay, gene expression analysis by real-time PCR and ELISA immunoassay for the detection of prostaglandin E2 (PGE2), interleukin 8 (IL8) and stromelysin-1 (MMP3), respectively. Dinoprostone 333-349 tumor necrosis factor Homo sapiens 42-63 24349530-5 2013 RESULTS: Inhibitors of cPLA2alpha enzyme activity (AVX002, ATK) significantly reduced TNF-induced cellular release of AA, PGE2, IL8 and MMP3. Dinoprostone 122-126 tumor necrosis factor Homo sapiens 86-89 26069676-9 2013 Linoleic acid increased PGE2 production in the presence of TNFalpha. Dinoprostone 24-28 tumor necrosis factor Homo sapiens 59-67 23876538-13 2013 Tumor necrosis factor alpha-induced COX-2 expression and PGE2 synthesis were also inhibited. Dinoprostone 57-61 tumor necrosis factor Homo sapiens 0-27 24069158-3 2013 PRINCIPAL FINDINGS: We demonstrated that TNF-alpha induced cPLA2 mRNA and protein expression, promoter activity, and PGE2 secretion in HPAEpiCs. Dinoprostone 117-121 tumor necrosis factor Homo sapiens 41-50 23864609-9 2013 IL-1beta and TNF-alpha enhanced the production of PGE2. Dinoprostone 50-54 tumor necrosis factor Homo sapiens 13-22 23869759-5 2013 RESULTS: Our results indicated that TNFalpha, a powerful inflammatory cytokine, strongly promoted COX-2 expression and PGE2 production in colon cancer-associated fibroblasts. Dinoprostone 119-123 tumor necrosis factor Homo sapiens 36-44 23913961-13 2013 In GAS-infected human THP-1 (macrophage-like) cells, PGE2 inhibited the production of MCP-1 and TNF-alpha while augmenting IL-10 expression. Dinoprostone 53-57 tumor necrosis factor Homo sapiens 96-105 23971009-2 2013 Upon stimulation by various proinflammatory stimuli such as lipopolysaccharide (LPS), interleukin (IL)-1beta, and tumor necrosis factor (TNF)-alpha, PGE2 synthesis is upregulated by the expression of cyclooxygenases. Dinoprostone 149-153 tumor necrosis factor Homo sapiens 114-147 22561311-3 2012 We have previously reported that defined cocktails of cytokines, involving TNFalpha and IFNgamma, induce mature type-1 polarized DCs (DC1s) which produce strongly elevated levels of IL-12 and CXCL10/IP10 upon CD40 ligation compared to "standard" PGE2-matured DCs (sDCs; matured with IL-1beta, IL-6, TNFalpha, and PGE2) and show higher CTL-inducing activity. Dinoprostone 246-250 tumor necrosis factor Homo sapiens 75-83 24715949-6 2013 Interferon gamma (IFN-gamma) and tumour necrosis factor alpha (TNF-alpha) play crucial roles in the initial activation of HIDEMs and importantly indoleamine 2,3 dioxygenase (IDO) and prostaglandin E2 (PGE-2) were identified as key mechanisms involved in HIDEM suppression of T cell proliferation. Dinoprostone 183-199 tumor necrosis factor Homo sapiens 63-72 24715949-6 2013 Interferon gamma (IFN-gamma) and tumour necrosis factor alpha (TNF-alpha) play crucial roles in the initial activation of HIDEMs and importantly indoleamine 2,3 dioxygenase (IDO) and prostaglandin E2 (PGE-2) were identified as key mechanisms involved in HIDEM suppression of T cell proliferation. Dinoprostone 201-206 tumor necrosis factor Homo sapiens 63-72 22977257-4 2012 Although PGE2 does not induce IL-23p19 expression by itself, it synergizes with both extra- and intracellular Toll-like receptor ligands and with inflammatory cytokines such as TNFalpha. Dinoprostone 9-13 tumor necrosis factor Homo sapiens 177-185 22977257-5 2012 We established that the effect of PGE2 in conjunction with either LPS or TNFalpha is mediated through the EP4 receptor and the cAMP-dependent activation of both protein kinase A (PKA) and exchange protein activated by cAMP (EPAC). Dinoprostone 34-38 tumor necrosis factor Homo sapiens 73-81 22561311-3 2012 We have previously reported that defined cocktails of cytokines, involving TNFalpha and IFNgamma, induce mature type-1 polarized DCs (DC1s) which produce strongly elevated levels of IL-12 and CXCL10/IP10 upon CD40 ligation compared to "standard" PGE2-matured DCs (sDCs; matured with IL-1beta, IL-6, TNFalpha, and PGE2) and show higher CTL-inducing activity. Dinoprostone 313-317 tumor necrosis factor Homo sapiens 75-83 22332123-9 2012 RESULTS: SFN inhibited the production of PGE2 and NO induced by IL-1beta and TNF-alpha. Dinoprostone 41-45 tumor necrosis factor Homo sapiens 77-86 21737776-8 2011 TNF-alpha increased small intestinal mucus secretion and goblet cell hypersensitivity to prostaglandin E2 (PGE(2)), a known mucus secretagogue produced by macrophages. Dinoprostone 89-105 tumor necrosis factor Homo sapiens 0-9 22008910-5 2012 A third mode of action is to create a second negative feedback loop whereby lipopolysaccharide, TNF-alpha, nitric oxide, and perhaps other damage-associated molecular patterns (DAMPs) from injured tissues and macrophages activate MSCs to secrete prostaglandin E(2) (PGE(2)). Dinoprostone 246-264 tumor necrosis factor Homo sapiens 96-105 21546578-0 2011 Counteracting effect of TRPC1-associated Ca2+ influx on TNF-alpha-induced COX-2-dependent prostaglandin E2 production in human colonic myofibroblasts. Dinoprostone 90-106 tumor necrosis factor Homo sapiens 56-65 21481814-7 2011 Results showed that in freshly isolated human monocytes, both the beta(2)-agonists and PGE(2) significantly inhibited LPS-induced TNF-alpha release as well as increased intracellular cAMP. Dinoprostone 87-93 tumor necrosis factor Homo sapiens 130-139 21546578-10 2011 In aggregate, these results strongly suggest that, in colonic myofibroblasts, NF-kappaB and NFAT serve as important positive and negative transcriptional regulators of TNF-alpha-induced COX-2-dependent PGE(2) production, respectively, at the downstream of TRPC1-associated Ca(2+) influx. Dinoprostone 202-208 tumor necrosis factor Homo sapiens 168-177 21635971-7 2011 The results showed that PGE2 inhibited IFN-gamma, TNF-alpha and IL-4 production by CD4+ T cells 24h after cell culture. Dinoprostone 24-28 tumor necrosis factor Homo sapiens 50-59 21178846-17 2011 IL-6 + sR also enhanced IL-1 and TNF-alpha stimulated synthesis of PGE-2. Dinoprostone 67-72 tumor necrosis factor Homo sapiens 33-42 21217452-8 2011 RESULTS: Across all patients, TNF-alpha induced large, statistically significant increases in NO, PGE2, and IL6 secretion from IVD cells compared with controls (60-, 112-, and 4-fold increases, respectively; P < 0.0001). Dinoprostone 98-102 tumor necrosis factor Homo sapiens 30-39 21217452-9 2011 Coincubation of TNF-alpha with nanomolar doses of sTNFRII significantly attenuated the secretion of NO and PGE2 in a dose-dependent manner, whereas IL6 levels were unchanged. Dinoprostone 107-111 tumor necrosis factor Homo sapiens 16-25 21511722-6 2011 TNF-alpha treatment significantly up-regulated the levels of PGE2, NO, sICAM-1, TGF-beta1, MCP-1, and MIP-1alpha in the supernatants of RASFs, increased the protein expression of COX-2, iNOS, and induced phosphorylation of Akt, IkappaB-alpha, NFkappaB, and ERK1/2 in RASFs. Dinoprostone 61-65 tumor necrosis factor Homo sapiens 0-9 20832511-5 2011 TNF-alpha stimulated expression of COX-2 and PG E synthase before that of TNAP, but expression of PG D synthase later suggesting that PGE2 and PGF2alpha but not 15d-PGJ2 were involved in TNF-alpha effects. Dinoprostone 134-138 tumor necrosis factor Homo sapiens 187-196 21760774-7 2011 There was a significant increase in the migration of BxPC-3 cells with TNF-alpha, LPS, or PGE(2) treatment; however, the increase caused by TNF-alpha or LPS was also inhibited remarkably by NS398. Dinoprostone 90-96 tumor necrosis factor Homo sapiens 140-149 20832511-5 2011 TNF-alpha stimulated expression of COX-2 and PG E synthase before that of TNAP, but expression of PG D synthase later suggesting that PGE2 and PGF2alpha but not 15d-PGJ2 were involved in TNF-alpha effects. Dinoprostone 134-138 tumor necrosis factor Homo sapiens 0-9 21417548-9 2011 IL-1beta and TNF strongly increased PGE2 production, with IL-1beta as the most prominent inducer. Dinoprostone 36-40 tumor necrosis factor Homo sapiens 13-16 19697035-0 2010 Differential effect of IL-1beta and TNFalpha on the production of IL-6, IL-8 and PGE2 in fibroblast-like synoviocytes and THP-1 macrophages. Dinoprostone 81-85 tumor necrosis factor Homo sapiens 36-44 21129557-8 2010 RESULTS: Eicosapentaenoic acid effectively reduced LPS-induced or PGE(2)-induced TNF-alpha and IL-6 expression, and increased IL-10 expression significantly when compared with arachidonic acid. Dinoprostone 66-72 tumor necrosis factor Homo sapiens 81-90 20616214-0 2010 Oxytocin and tumor necrosis factor alpha stimulate expression of prostaglandin E2 synthase and secretion of prostaglandin E2 by luminal epithelial cells of the porcine endometrium during early pregnancy. Dinoprostone 65-81 tumor necrosis factor Homo sapiens 13-40 20616214-5 2010 TNF stimulated PTGS2 and mPGES-1 mRNA, as well as mPGES-1 protein expression and PGE(2) release on days 11-12 of pregnancy and the estrous cycle. Dinoprostone 81-87 tumor necrosis factor Homo sapiens 0-3 20616214-8 2010 This study indicates that TNF and OXT regulate PGE(2) synthesis in LECs during early pregnancy. Dinoprostone 47-53 tumor necrosis factor Homo sapiens 26-29 20815659-1 2010 The inflammatory cytokines tumor necrosis factor alpha (TNFalpha) and interferon gamma (IFNgamma) stimulate production of the inflammatory mediators prostaglandin E2 (PGEgamma), prostacyclin (PGIgamma), and nitric oxide (NO) in cultured lung epithelial cells. Dinoprostone 149-165 tumor necrosis factor Homo sapiens 27-54 20815659-1 2010 The inflammatory cytokines tumor necrosis factor alpha (TNFalpha) and interferon gamma (IFNgamma) stimulate production of the inflammatory mediators prostaglandin E2 (PGEgamma), prostacyclin (PGIgamma), and nitric oxide (NO) in cultured lung epithelial cells. Dinoprostone 149-165 tumor necrosis factor Homo sapiens 56-64 20815659-3 2010 Primary bronchiolar epithelial Clara cells treated with TNFalpha and IFNgamma also produced increased PGE2, PGI2, and NO, and PG and NO production was decreased by MEK inhibition. Dinoprostone 102-106 tumor necrosis factor Homo sapiens 56-64 20206688-2 2010 The NF-kappaB-dependent gene expression of IL8, IL6, PTGS2/COX2, TNF and IL33 in directly irradiated human skin fibroblasts produced the cytokines and prostaglandin E2 (PGE2) with autocrine/paracrine functions, which further activated signaling pathways and induced NF-kappaB-dependent gene expression in bystander cells. Dinoprostone 151-167 tumor necrosis factor Homo sapiens 65-68 20064200-9 2010 Furthermore, we found a significant time-dependent upregulation of prostaglandin E2 synthesis upon TNF-alpha treatment. Dinoprostone 67-83 tumor necrosis factor Homo sapiens 99-108 20398340-13 2010 The involvement of the signal pathways JNK and NF-kappaB in the regulation of PGE2 induced by TNFalpha may suggest these two pathways as possible attractive targets in the chronic inflammatory disease periodontitis. Dinoprostone 78-82 tumor necrosis factor Homo sapiens 94-102 20398340-2 2010 We have previously shown that tumor necrosis factor alpha (TNFalpha) induces PGE2 synthesis in gingival fibroblasts. Dinoprostone 77-81 tumor necrosis factor Homo sapiens 30-57 20398340-2 2010 We have previously shown that tumor necrosis factor alpha (TNFalpha) induces PGE2 synthesis in gingival fibroblasts. Dinoprostone 77-81 tumor necrosis factor Homo sapiens 59-67 20398340-3 2010 In this study we aimed to investigate the global gene expression profile of TNFalpha-stimulated primary human gingival fibroblasts, focusing on signal pathways related to the PGE2-synthesizing enzymes prostaglandin E synthases (PGES), as well as the upstream enzyme cyclooxygenase-2 (COX-2) and PGE2 production. Dinoprostone 175-179 tumor necrosis factor Homo sapiens 76-84 20398340-3 2010 In this study we aimed to investigate the global gene expression profile of TNFalpha-stimulated primary human gingival fibroblasts, focusing on signal pathways related to the PGE2-synthesizing enzymes prostaglandin E synthases (PGES), as well as the upstream enzyme cyclooxygenase-2 (COX-2) and PGE2 production. Dinoprostone 295-299 tumor necrosis factor Homo sapiens 76-84 20398340-4 2010 RESULTS: Microarray and western blot analyses showed that the mRNA and protein expression of the inflammatory induced microsomal prostaglandin E synthase-1 (mPGES-1) was up-regulated by the cytokine TNFalpha, accompanied by enhanced expression of COX-2 and increased production of PGE2. Dinoprostone 281-285 tumor necrosis factor Homo sapiens 199-207 20398340-10 2010 Inhibitors of JNK and NF-kappaB also decreased the TNFalpha-stimulated up-regulation of mPGES-1 and COX-2 as well as PGE2 production. Dinoprostone 117-121 tumor necrosis factor Homo sapiens 51-59 20398340-12 2010 Inhibition of these TNFalpha-activated signal pathways reduced the expression of mPGES-1 and COX-2 as well as their end product PGE2 in gingival fibroblasts. Dinoprostone 128-132 tumor necrosis factor Homo sapiens 20-28 20064200-11 2010 CONCLUSIONS: Our results provide evidence that TNF-alpha specifically modulates the function of MFs through regulation of prostaglandin E2 synthesis and therefore may play a crucial role in the pathogenesis of joint capsule contractures. Dinoprostone 122-138 tumor necrosis factor Homo sapiens 47-56 20659035-7 2010 Moreover addition of exogenous MCP 1 and prostaglandin E2 elevates synthesis of MMP 1, TNF alpha, and GM CSF by monocytes. Dinoprostone 41-57 tumor necrosis factor Homo sapiens 87-96 20067543-2 2009 Here we demonstrate that tumour-derived prostaglandin E2 (PGE(2)) and transforming growth factor-beta (TGF-beta) increase interleukin-8 (IL-8) but synergistically inhibit interferon-alpha (IFN-alpha) and tumour necrosis factor (TNF) production of Toll-like receptor 7 (TLR7)- and Toll-like receptor 9 (TLR9)-stimulated PDC. Dinoprostone 40-56 tumor necrosis factor Homo sapiens 204-226 21370737-8 2010 TNFalpha at a dose of 1 ng/ml significantly increased PGF2alpha secretion at estrus (P < 0.01) and PGE2 secretion at diestrus (P < 0.001) after 12h incubation. Dinoprostone 102-106 tumor necrosis factor Homo sapiens 0-8 20067543-2 2009 Here we demonstrate that tumour-derived prostaglandin E2 (PGE(2)) and transforming growth factor-beta (TGF-beta) increase interleukin-8 (IL-8) but synergistically inhibit interferon-alpha (IFN-alpha) and tumour necrosis factor (TNF) production of Toll-like receptor 7 (TLR7)- and Toll-like receptor 9 (TLR9)-stimulated PDC. Dinoprostone 40-56 tumor necrosis factor Homo sapiens 228-231 19109223-9 2009 TNF decreased FM rupture strength 50% while increasing MMP9 and PGE(2) release. Dinoprostone 64-70 tumor necrosis factor Homo sapiens 0-3 19542367-0 2009 Prostaglandin E2 differentially modulates proinflammatory/prodestructive effects of TNF-alpha on synovial fibroblasts via specific E prostanoid receptors/cAMP. Dinoprostone 0-16 tumor necrosis factor Homo sapiens 84-93 19201813-8 2009 Collectively, our data for the first time suggest a dual role of ozone in modulating IL-6 secretion and TEER outcomes in a PGE(2)-dependent (in presence of TNF stimulus) and -independent manner (in absence of cytokine stimulus). Dinoprostone 123-129 tumor necrosis factor Homo sapiens 156-159 19218340-9 2009 In conclusion, we propose a novel signaling pathway of MMP-9 up-regulation in CC cells such that TNF-alpha induces the activation of COX-2 and PGE2 via TNF-R1 followed by the up-regulation of MMP-9 via the PGE2 (EP2/4) receptor. Dinoprostone 143-147 tumor necrosis factor Homo sapiens 97-106 19218340-9 2009 In conclusion, we propose a novel signaling pathway of MMP-9 up-regulation in CC cells such that TNF-alpha induces the activation of COX-2 and PGE2 via TNF-R1 followed by the up-regulation of MMP-9 via the PGE2 (EP2/4) receptor. Dinoprostone 206-210 tumor necrosis factor Homo sapiens 97-106 18327580-3 2008 RESULTS: PGE2 and adenosine inhibited LAK cells cytotoxic activity and production of INF-gamma, GM-CSF and TNF-alpha. Dinoprostone 9-13 tumor necrosis factor Homo sapiens 107-116 18562219-8 2009 RESULTS: Over-expression of a dominant negative MK2 inhibited HSP27 phosphorylation and significantly reduced both interleukin 1 (IL-1)beta and tumour necrosis factor (TNF)-alpha mediated release of PGE2 in HeLa cells over a 24h period. Dinoprostone 199-203 tumor necrosis factor Homo sapiens 144-178 18996481-9 2008 7beta-OH-EPIA alone had no effect on PGE2 biosynthesis but suppressed TNF-alpha-induced PGE2 circa 50%. Dinoprostone 88-92 tumor necrosis factor Homo sapiens 70-79 18288087-1 2008 Tumor necrosis factor-alpha (TNF-alpha) has a central role in inflammation and is modulated by prostaglandin E(2) (PGE(2)) and cyclic adenosine monophosphate (cAMP). Dinoprostone 95-113 tumor necrosis factor Homo sapiens 0-27 18417374-9 2008 IL-17- and tumor necrosis factor-alpha (TNF-alpha)-induced NO and PGE(2) production was also inhibited by TSA and BA. Dinoprostone 66-72 tumor necrosis factor Homo sapiens 40-49 18288087-1 2008 Tumor necrosis factor-alpha (TNF-alpha) has a central role in inflammation and is modulated by prostaglandin E(2) (PGE(2)) and cyclic adenosine monophosphate (cAMP). Dinoprostone 95-113 tumor necrosis factor Homo sapiens 29-38 18295521-5 2008 Activation of the monocyte ETB subtype by ET (1 ng/ml) concentration-dependently stimulated TNF-alpha (744%) >PGE2 (570%) > IL-1 beta (112%) and had no effect on 5-lipoxygenase metabolism. Dinoprostone 113-117 tumor necrosis factor Homo sapiens 92-101 18481385-3 2008 Here, we demonstrate that DCs matured with TNF-alpha alone or in combination with CD40 agonism are highly deficient, both physiologically and functionally, in comparison with DCs matured with IL-1beta, TNF-alpha, IL-6, and prostaglandin E2. Dinoprostone 223-239 tumor necrosis factor Homo sapiens 43-52 21141574-0 2008 [TNF-alpha upregulate MUC5AC mucin secretion through COX2/PGE2 mechanism]. Dinoprostone 58-62 tumor necrosis factor Homo sapiens 1-10 17485421-9 2008 When prostaglandin-E2 was added, in addition to IL-1beta+TNFalpha, proteoglycan release increased further, but proteoglycan synthesis was not influenced further. Dinoprostone 5-21 tumor necrosis factor Homo sapiens 57-65 17485421-10 2008 Addition of a selective COX-2 inhibitor to the IL-1beta+TNFalpha treated cartilage inhibited the enhanced prostaglandin-E2 production and almost completely normalised proteoglycan release, whereas synthesis remained unaffected. Dinoprostone 106-122 tumor necrosis factor Homo sapiens 56-64 17485421-14 2008 IL-1beta+TNFalpha induced NO seems to be involved in inhibition of proteoglycan synthesis, independent of prostaglandin-E2, and thus seems insensitive to regulation by (selective) COX-2 inhibitors. Dinoprostone 106-122 tumor necrosis factor Homo sapiens 9-17 18007587-4 2008 Downregulation of Hsp27 using Hsp27-specific small interfering RNA increased prostaglandin E(2) (PGE(2)) production in both unstimulated and tumor necrosis factor-alpha (TNF-alpha)-stimulated keratinocytes. Dinoprostone 77-95 tumor necrosis factor Homo sapiens 141-168 18007587-4 2008 Downregulation of Hsp27 using Hsp27-specific small interfering RNA increased prostaglandin E(2) (PGE(2)) production in both unstimulated and tumor necrosis factor-alpha (TNF-alpha)-stimulated keratinocytes. Dinoprostone 77-95 tumor necrosis factor Homo sapiens 170-179 18007587-4 2008 Downregulation of Hsp27 using Hsp27-specific small interfering RNA increased prostaglandin E(2) (PGE(2)) production in both unstimulated and tumor necrosis factor-alpha (TNF-alpha)-stimulated keratinocytes. Dinoprostone 97-103 tumor necrosis factor Homo sapiens 141-168 18007587-4 2008 Downregulation of Hsp27 using Hsp27-specific small interfering RNA increased prostaglandin E(2) (PGE(2)) production in both unstimulated and tumor necrosis factor-alpha (TNF-alpha)-stimulated keratinocytes. Dinoprostone 97-103 tumor necrosis factor Homo sapiens 170-179 18060853-0 2008 Prostaglandin E2 inhibits tumor necrosis factor-alpha RNA through PKA type I. Dinoprostone 0-16 tumor necrosis factor Homo sapiens 26-53 18295521-6 2008 Compared with ET a different profile of IL-1 beta >TNF-alpha >PGE2 was induced by LPS. Dinoprostone 68-72 tumor necrosis factor Homo sapiens 54-63 17499749-0 2007 TNF-alpha modulates hepatic Na+-K+ ATPase activity via PGE2 and EP2 receptors. Dinoprostone 55-59 tumor necrosis factor Homo sapiens 0-9 18671915-8 2008 In TNF- or spermine-treated endometria, the expression of prostaglandin (PG) E(2) increased in the early and mid-luteal phases, whereas that of PGF(2alpha) increased in the follicular and late luteal phases. Dinoprostone 58-81 tumor necrosis factor Homo sapiens 3-6 18246004-10 2007 Blocking cytokine activation of p38 MAPK reduced IL-1 and TNF-alpha induced PGE2 and IL-6 accumulation. Dinoprostone 76-80 tumor necrosis factor Homo sapiens 58-67 17707523-4 2007 The cytokines TNFalpha and IL-1beta increased protein expression and activity of mPGES-1, accompanied by increased COX-2 expression and PGE2 production. Dinoprostone 136-140 tumor necrosis factor Homo sapiens 14-22 17669557-5 2007 Among them, production of prostaglandin E(2) (PGE(2)), via B(1) receptors in primary cultured microglia, has a negative feedback effect on lipopolysaccharide (LPS)-induced release of tumor necrosis factor-alpha (TNF-alpha) via increasing intracellular cyclic adenosine monophosphate (cAMP). Dinoprostone 26-44 tumor necrosis factor Homo sapiens 183-210 17669557-5 2007 Among them, production of prostaglandin E(2) (PGE(2)), via B(1) receptors in primary cultured microglia, has a negative feedback effect on lipopolysaccharide (LPS)-induced release of tumor necrosis factor-alpha (TNF-alpha) via increasing intracellular cyclic adenosine monophosphate (cAMP). Dinoprostone 26-44 tumor necrosis factor Homo sapiens 212-221 17669557-5 2007 Among them, production of prostaglandin E(2) (PGE(2)), via B(1) receptors in primary cultured microglia, has a negative feedback effect on lipopolysaccharide (LPS)-induced release of tumor necrosis factor-alpha (TNF-alpha) via increasing intracellular cyclic adenosine monophosphate (cAMP). Dinoprostone 46-52 tumor necrosis factor Homo sapiens 183-210 17669557-5 2007 Among them, production of prostaglandin E(2) (PGE(2)), via B(1) receptors in primary cultured microglia, has a negative feedback effect on lipopolysaccharide (LPS)-induced release of tumor necrosis factor-alpha (TNF-alpha) via increasing intracellular cyclic adenosine monophosphate (cAMP). Dinoprostone 46-52 tumor necrosis factor Homo sapiens 212-221 17557348-13 2007 The potent TNF-alpha inhibitory activity found at day 6 after injury correlated with increased levels of PGE2 and indicates cell-mediated hyporesponsiveness to a second stimulus. Dinoprostone 105-109 tumor necrosis factor Homo sapiens 11-20 18219763-6 2007 IL-17 binding to an IL-17 receptor expressed on epithelial, endothelial, and fibroblastic stromal cells triggers the activation of transcription factor NF-kappaB and mitogen-activated protein kinase (p-38), which in turn results in the secretion of IL-1, TNF-alpha, IL-6, IL-8, or prostaglandin E2. Dinoprostone 281-297 tumor necrosis factor Homo sapiens 255-264 17300864-0 2007 Aldose reductase regulates TNF-alpha-induced PGE2 production in human colon cancer cells. Dinoprostone 45-49 tumor necrosis factor Homo sapiens 27-36 17300864-3 2007 Herein we report that inhibition/antisense abolition of polyol pathway enzyme, aldose reductase (AR) inhibited the TNF-alpha-induced synthesis of prostaglandin E2 and the activity of cyclooxygenase (Cox) in human colon cancer cells, Caco-2. Dinoprostone 146-162 tumor necrosis factor Homo sapiens 115-124 17499749-4 2007 This effect disappeared in presence of indomethacin, an inhibitor of COX enzymes, and PGE2 injected to the animals imitated the effect of TNF-alpha. Dinoprostone 86-90 tumor necrosis factor Homo sapiens 138-147 17499749-7 2007 It was concluded that TNF-alpha induces in hepatocytes, PGE2 production which in turn reduces the activity and protein expression of the Na(+)-K(+) ATPase by activating EP2 receptors. Dinoprostone 56-60 tumor necrosis factor Homo sapiens 22-31 17400014-3 2007 Thus, the purpose of this work was to determine whether the effect of PGE2 in fungicidal activity was related with decrease on H(2)O(2) release, the metabolite involved in P. brasiliensis killing, and changes in the levels of TNF-alpha, IL-6 and IL-10. Dinoprostone 70-74 tumor necrosis factor Homo sapiens 226-235 17400014-4 2007 Human monocytes challenged with the fungus produced high PGE2 levels, which in turn inhibited the fungicidal activity of these cells by reducing H(2)O(2) and TNF-alpha production. Dinoprostone 57-61 tumor necrosis factor Homo sapiens 158-167 17178880-5 2006 PGE2 and BK triggered EGFR signaling by increasing selective autocrine release of transforming growth factor-alpha (TGF-alpha). Dinoprostone 0-4 tumor necrosis factor Homo sapiens 82-114 17683641-11 2007 Real-time PCR analysis of articular cartilage from five patients with OA revealed that PGE2 at 10 pg/ml suppressed the expression of matrix metalloproteinase (MMP)-13 and to a smaller extent MMP-1, as well as the proinflammatory cytokines IL-1beta and TNF-alpha and type X collagen (COL10A1), the last of these being a marker of chondrocyte hypertrophy. Dinoprostone 87-91 tumor necrosis factor Homo sapiens 252-261 17031853-0 2007 Prostaglandin E2 downregulates TNF-alpha-induced production of matrix metalloproteinase-1 in HCS-2/8 chondrocytes by inhibiting Raf-1/MEK/ERK cascade through EP4 prostanoid receptor activation. Dinoprostone 0-16 tumor necrosis factor Homo sapiens 31-40 17214584-5 2006 PGE2 is also produced in response to proinflammatory cytokines, which in turn negatively regulates both IL-17 and TNF-alpha expression and TNF/IL-1-induced activation of fibroblast-like synoviocytes through EP2/EP4 receptors, resulting in the modulation of proinflammatory cascades. Dinoprostone 0-4 tumor necrosis factor Homo sapiens 114-123 17214584-5 2006 PGE2 is also produced in response to proinflammatory cytokines, which in turn negatively regulates both IL-17 and TNF-alpha expression and TNF/IL-1-induced activation of fibroblast-like synoviocytes through EP2/EP4 receptors, resulting in the modulation of proinflammatory cascades. Dinoprostone 0-4 tumor necrosis factor Homo sapiens 114-117 16784723-6 2006 Anti-prostaglandin E2 (PGE2) antiserum or antisense oligonucleotides against PGE2 receptor EP2 or EP3 abrogated inhibitory effects of ketoconazole and terbinafine hydrochloride on TNF-alpha-induced NF-kappaB activity and CCL27, CCL2, and CCL5 production, indicating the involvement of endogenous PGE2 in the inhibitory effects. Dinoprostone 77-81 tumor necrosis factor Homo sapiens 180-189 16784723-6 2006 Anti-prostaglandin E2 (PGE2) antiserum or antisense oligonucleotides against PGE2 receptor EP2 or EP3 abrogated inhibitory effects of ketoconazole and terbinafine hydrochloride on TNF-alpha-induced NF-kappaB activity and CCL27, CCL2, and CCL5 production, indicating the involvement of endogenous PGE2 in the inhibitory effects. Dinoprostone 5-21 tumor necrosis factor Homo sapiens 180-189 16784723-6 2006 Anti-prostaglandin E2 (PGE2) antiserum or antisense oligonucleotides against PGE2 receptor EP2 or EP3 abrogated inhibitory effects of ketoconazole and terbinafine hydrochloride on TNF-alpha-induced NF-kappaB activity and CCL27, CCL2, and CCL5 production, indicating the involvement of endogenous PGE2 in the inhibitory effects. Dinoprostone 23-27 tumor necrosis factor Homo sapiens 180-189 16948668-11 2006 CONCLUSIONS: Interleukin-1beta and TNF-alpha may stimulate PGE(2) production in dental pulp cells. Dinoprostone 59-65 tumor necrosis factor Homo sapiens 35-44 16803890-0 2006 Acid ceramidase but not acid sphingomyelinase is required for tumor necrosis factor-{alpha}-induced PGE2 production. Dinoprostone 100-104 tumor necrosis factor Homo sapiens 62-90 16803890-6 2006 In this study, the requirement for acid sphingomyelinase and sphingomyelin metabolites in the TNFalpha/prostaglandin E(2) (PGE(2)) pathway was investigated. Dinoprostone 103-121 tumor necrosis factor Homo sapiens 94-102 16784723-10 2006 These results suggest that ketoconazole and terbinafine hydrochloride may suppress TNF-alpha-induced NF-kappaB activity and CCL27, CCL2, and CCL5 production by increasing PGE2 release from keratinocytes. Dinoprostone 171-175 tumor necrosis factor Homo sapiens 83-92 16619186-0 2006 Suppression of prostaglandin E2 by malaria parasite products and antipyretics promotes overproduction of tumor necrosis factor-alpha: association with the pathogenesis of childhood malarial anemia. Dinoprostone 15-31 tumor necrosis factor Homo sapiens 105-132 16816110-2 2006 We investigated the actions of TNFalpha toward stimulation of PGE2 synthesis in primary spinal cord neurons. Dinoprostone 62-66 tumor necrosis factor Homo sapiens 31-39 16816110-3 2006 TNFalpha induced COX-2 and mPGES-1 expression in neurons, followed by formation of PGE2, which was blocked by a selective COX-2 inhibitor. Dinoprostone 83-87 tumor necrosis factor Homo sapiens 0-8 16816110-4 2006 Surprisingly, the "selective COX-1" inhibitor SC-560 completely inhibited TNFalpha-induced PGE2 synthesis in neurons at nanomolar concentrations. Dinoprostone 91-95 tumor necrosis factor Homo sapiens 74-82 16816110-8 2006 Most importantly, SC-560 blocked TNFalpha-induced PGE2 synthesis in COX-1-deficient spinal cord neurons, demonstrating a COX-1-independent inhibition of PGE2 synthesis. Dinoprostone 50-54 tumor necrosis factor Homo sapiens 33-41 16619186-2 2006 Tumor necrosis factor (TNF)-alpha limits malaria parasitemia but also promotes pathogenesis at high concentrations, whereas prostaglandin E2 (PGE2) inhibits TNF-alpha production and is reduced in childhood malaria, at least in part, through suppression of cyclooxygenase (COX)-2 following the ingestion of Plasmodium falciparum hemozoin (pfHz; malarial pigment) by peripheral blood mononuclear cells (PBMCs). Dinoprostone 124-140 tumor necrosis factor Homo sapiens 157-166 16619186-2 2006 Tumor necrosis factor (TNF)-alpha limits malaria parasitemia but also promotes pathogenesis at high concentrations, whereas prostaglandin E2 (PGE2) inhibits TNF-alpha production and is reduced in childhood malaria, at least in part, through suppression of cyclooxygenase (COX)-2 following the ingestion of Plasmodium falciparum hemozoin (pfHz; malarial pigment) by peripheral blood mononuclear cells (PBMCs). Dinoprostone 142-146 tumor necrosis factor Homo sapiens 157-166 16619186-4 2006 Moreover, addition of exogenous PGE2 to pfHz-treated PBMCs dose-dependently decreased TNF-alpha production, whereas experimental COX inhibitors and antipyretics used during human malaria generated increased TNF-alpha production. Dinoprostone 32-36 tumor necrosis factor Homo sapiens 86-95 16619186-6 2006 The results of the present study illustrate that pfHz-induced suppression of PGE2 promotes overproduction of TNF-alpha, which is associated with enhanced malarial anemia. Dinoprostone 77-81 tumor necrosis factor Homo sapiens 109-118 16491333-4 2006 As an example, released inflammatory cytokines (e.g., interleukin-1 beta (IL-1 beta) and tumor necrosis factor-alpha (TNF-alpha)), activated in up-stream macrophages, flow through a microfluidic mixing system, generating linear concentration gradients in down-stream wells and inducing down-stream osteoblasts to release prostaglandin E2 (PGE2), a well-known bone resorption marker. Dinoprostone 321-337 tumor necrosis factor Homo sapiens 118-127 16357326-4 2006 PGE2 stimulated the accumulation of cyclic adenosine monophosphate (cAMP), and suppressed both Fc epsilonRI-mediated eicosanoid production and tumor necrosis factor-alpha (TNF-alpha) generation. Dinoprostone 0-4 tumor necrosis factor Homo sapiens 143-170 16357326-4 2006 PGE2 stimulated the accumulation of cyclic adenosine monophosphate (cAMP), and suppressed both Fc epsilonRI-mediated eicosanoid production and tumor necrosis factor-alpha (TNF-alpha) generation. Dinoprostone 0-4 tumor necrosis factor Homo sapiens 172-181 16424369-7 2006 Interference with EPRAP function by small interference RNA limited prostaglandin E2-mediated suppression of chemokine expression in macrophages activated with lipopolysaccharide and tumor necrosis factor alpha. Dinoprostone 67-83 tumor necrosis factor Homo sapiens 182-209 16508938-11 2006 Moreover, S1P enhanced expression of COX-2 and production of PGE2 induced by stimulation with TNFalpha or IL-1beta in RA synoviocytes and MH7A cells. Dinoprostone 61-65 tumor necrosis factor Homo sapiens 94-102 16491333-4 2006 As an example, released inflammatory cytokines (e.g., interleukin-1 beta (IL-1 beta) and tumor necrosis factor-alpha (TNF-alpha)), activated in up-stream macrophages, flow through a microfluidic mixing system, generating linear concentration gradients in down-stream wells and inducing down-stream osteoblasts to release prostaglandin E2 (PGE2), a well-known bone resorption marker. Dinoprostone 339-343 tumor necrosis factor Homo sapiens 118-127 16399672-2 2006 Activation of these receptors by transforming growth factor alpha (TGFalpha) results in production of prostaglandin E2, which then stimulates luteinizing hormone releasing hormone (LHRH) neurons to secrete LHRH, the neuropeptide controlling sexual development. Dinoprostone 102-118 tumor necrosis factor Homo sapiens 33-65 16428068-5 2006 Tumor necrosis factor-alpha (TNF-alpha) and granulocyte-macrophage colony-stimulating factor (GM-CSF) enhanced prostaglandin E2 (PGE2) release through the induction of COX-2 in neutrophils. Dinoprostone 111-127 tumor necrosis factor Homo sapiens 0-27 16428068-5 2006 Tumor necrosis factor-alpha (TNF-alpha) and granulocyte-macrophage colony-stimulating factor (GM-CSF) enhanced prostaglandin E2 (PGE2) release through the induction of COX-2 in neutrophils. Dinoprostone 111-127 tumor necrosis factor Homo sapiens 29-38 16428068-5 2006 Tumor necrosis factor-alpha (TNF-alpha) and granulocyte-macrophage colony-stimulating factor (GM-CSF) enhanced prostaglandin E2 (PGE2) release through the induction of COX-2 in neutrophils. Dinoprostone 129-133 tumor necrosis factor Homo sapiens 0-27 16428068-5 2006 Tumor necrosis factor-alpha (TNF-alpha) and granulocyte-macrophage colony-stimulating factor (GM-CSF) enhanced prostaglandin E2 (PGE2) release through the induction of COX-2 in neutrophils. Dinoprostone 129-133 tumor necrosis factor Homo sapiens 29-38 16428068-7 2006 TNF-alpha-and GM-CSF-induced PGE2 release was blocked by the addition of the selective COX-2 inhibitor, N-(2-cyclohexyloxy-4-nitrophenyl)-methanesulfonamide (NS-398; 1 microM). Dinoprostone 29-33 tumor necrosis factor Homo sapiens 0-9 16244112-8 2006 Moreover, addition of exogenous MCP-1 or PGE2 enhanced MMP-1 production by TNF-alpha- and GM-CSF-stimulated monocytes. Dinoprostone 41-45 tumor necrosis factor Homo sapiens 75-84 16244114-14 2006 IL-1beta and tumor necrosis factor alpha were also found to potentiate PGE-2 action. Dinoprostone 71-76 tumor necrosis factor Homo sapiens 13-40 16303787-1 2005 Prostaglandin E2 (PGE2) acts in synergy with other inflammatory stimuli such as tumor necrosis factor (TNF) to induce the maturation of migratory-type monocyte-derived dendritic cells (MoDCs). Dinoprostone 0-16 tumor necrosis factor Homo sapiens 103-106 16303787-3 2005 We demonstrate here that the addition of PGE2 to TNF for the maturation of MoDCs enhanced CD4 and CD8 T cell proliferative responses to neoantigen and recall antigen, and enhanced Th1-type responses. Dinoprostone 41-45 tumor necrosis factor Homo sapiens 49-52 16275389-11 2005 IL-17 alone or synergistically with TNF-alpha increased prostaglandin E(2) release from keratinocytes, and the increase was suppressed by NS398. Dinoprostone 56-74 tumor necrosis factor Homo sapiens 36-45 16123309-7 2005 Treatment of TNF-alpha-stimulated HT29 cells with EGCG dose-dependently inhibited the synthesis of IL-8, MIP-3alpha, and PGE2. Dinoprostone 121-125 tumor necrosis factor Homo sapiens 13-22 16255020-3 2005 METHODS: In vitro effects of TNF blockers and dexamethasone on the PGE(2) biosynthetic pathway were examined in RA synovial fluid mononuclear cells (SFMCs) by flow cytometry. Dinoprostone 67-73 tumor necrosis factor Homo sapiens 29-32 16255020-5 2005 Expression of enzymes responsible for PGE(2) synthesis ex vivo was evaluated by immunohistochemistry in synovial biopsy samples obtained from 18 patients before and after treatment with TNF blockers and from 16 patients before and after intraarticular treatment with glucocorticoids. Dinoprostone 38-44 tumor necrosis factor Homo sapiens 186-189 16272352-6 2005 PGE2 also blocked IL-1beta/TNF-alpha-stimulated ERK activation, and the ERK inhibitor, PD98059, mimicked PGE2 in blocking p65, but enhancing p50 nuclear translocation, suggesting that the effects of PGE2 on p65 and p50 are mediated via effects on ERK. Dinoprostone 0-4 tumor necrosis factor Homo sapiens 27-36 16272352-6 2005 PGE2 also blocked IL-1beta/TNF-alpha-stimulated ERK activation, and the ERK inhibitor, PD98059, mimicked PGE2 in blocking p65, but enhancing p50 nuclear translocation, suggesting that the effects of PGE2 on p65 and p50 are mediated via effects on ERK. Dinoprostone 105-109 tumor necrosis factor Homo sapiens 27-36 16272352-6 2005 PGE2 also blocked IL-1beta/TNF-alpha-stimulated ERK activation, and the ERK inhibitor, PD98059, mimicked PGE2 in blocking p65, but enhancing p50 nuclear translocation, suggesting that the effects of PGE2 on p65 and p50 are mediated via effects on ERK. Dinoprostone 105-109 tumor necrosis factor Homo sapiens 27-36 16253096-5 2005 RESULTS: PGE2 biosynthesis was dose dependently inhibited by both triclosan and triclosan and CPC when challenged by tumor necrosis factor (TNF)-alpha or interleukin (IL)-1beta. Dinoprostone 9-13 tumor necrosis factor Homo sapiens 117-150 15817699-7 2005 In contrast, the AT(2) antagonist inhibited the PGE(2) production induced by TNF-alpha and GM-CSF. Dinoprostone 48-54 tumor necrosis factor Homo sapiens 77-86 15843495-7 2005 We observed that COX2 expression and PGE2 production induced by tumor necrosis factor alpha (TNF) were significantly abrogated by 15d-PGJ2. Dinoprostone 37-41 tumor necrosis factor Homo sapiens 64-91 15843495-7 2005 We observed that COX2 expression and PGE2 production induced by tumor necrosis factor alpha (TNF) were significantly abrogated by 15d-PGJ2. Dinoprostone 37-41 tumor necrosis factor Homo sapiens 93-96 15843495-9 2005 Interestingly, treatment with ROSI, but not TRO, led to augmentation of TNF-stimulated PGE2 production. Dinoprostone 87-91 tumor necrosis factor Homo sapiens 72-75 15817699-8 2005 Ang II, through its interaction with the AT(2) receptor, has a central role in mediating the PGE(2)-dependent production of MMP-1 by monocytes stimulated with TNF-alpha and GM-CSF. Dinoprostone 93-99 tumor necrosis factor Homo sapiens 159-168 15851377-0 2005 FK506 enhances triptolide-induced down-regulation of cyclooxygenase-2, inducible nitric oxide synthase as well as their products PGE2 and NO in TNF-alpha-stimulated synovial fibroblasts from rheumatoid arthritic patients. Dinoprostone 129-133 tumor necrosis factor Homo sapiens 144-153 15772428-4 2005 We show that 1) tumor necrosis factor-alpha upregulates the expression of both COX-2 mRNA and prostaglandin E2 (PGE2) production, and 2) omega-3 and omega-6 PUFA regulate COX-2 mRNA expression and PGE2 production. Dinoprostone 112-116 tumor necrosis factor Homo sapiens 16-43 15772428-4 2005 We show that 1) tumor necrosis factor-alpha upregulates the expression of both COX-2 mRNA and prostaglandin E2 (PGE2) production, and 2) omega-3 and omega-6 PUFA regulate COX-2 mRNA expression and PGE2 production. Dinoprostone 197-201 tumor necrosis factor Homo sapiens 16-43 15772428-4 2005 We show that 1) tumor necrosis factor-alpha upregulates the expression of both COX-2 mRNA and prostaglandin E2 (PGE2) production, and 2) omega-3 and omega-6 PUFA regulate COX-2 mRNA expression and PGE2 production. Dinoprostone 94-110 tumor necrosis factor Homo sapiens 16-43 15649409-3 2005 Ethyl acetate chicory root extract produced a marked inhibition of prostaglandin E(2) (PGE(2)) production in human colon carcinoma HT29 cells treated with the pro-inflammatory agent TNF-alpha. Dinoprostone 67-85 tumor necrosis factor Homo sapiens 182-191 15640148-0 2005 Early growth response factor-1 mediates prostaglandin E2-dependent transcriptional suppression of cytokine-induced tumor necrosis factor-alpha gene expression in human macrophages and rheumatoid arthritis-affected synovial fibroblasts. Dinoprostone 40-56 tumor necrosis factor Homo sapiens 115-142 15649409-3 2005 Ethyl acetate chicory root extract produced a marked inhibition of prostaglandin E(2) (PGE(2)) production in human colon carcinoma HT29 cells treated with the pro-inflammatory agent TNF-alpha. Dinoprostone 87-93 tumor necrosis factor Homo sapiens 182-191 16040399-7 2005 The T-cell proliferative response to DC was enhanced by inclusion of PGE2 in the MCM-mimic (TNF-a, IL-1 a, IL-6, PGE2) cocktail. Dinoprostone 69-73 tumor necrosis factor Homo sapiens 92-97 15676206-2 2005 Prostaglandin E2 (PGE2), a member of the eicosanoid family of arachidonic acid derivatives, is widely used to enhance the TNF-alpha-driven maturation of human monocyte-derived DCs (moDCs) both in basic research and in clinical settings. Dinoprostone 0-16 tumor necrosis factor Homo sapiens 122-131 15676206-2 2005 Prostaglandin E2 (PGE2), a member of the eicosanoid family of arachidonic acid derivatives, is widely used to enhance the TNF-alpha-driven maturation of human monocyte-derived DCs (moDCs) both in basic research and in clinical settings. Dinoprostone 18-22 tumor necrosis factor Homo sapiens 122-131 15676206-4 2005 METHODS: In a side-by-side analysis we therefore compared the influence of PGE2 and PGA2 on the TNF-alpha-induced maturation of human moDCs. Dinoprostone 75-79 tumor necrosis factor Homo sapiens 96-105 15676206-6 2005 RESULTS: We found that PGA2 is nearly as potent as PGE2 in costimulating the TNF-alpha-induced phenotypic maturation of human moDCs. Dinoprostone 51-55 tumor necrosis factor Homo sapiens 77-86 15676206-7 2005 Both PGE2 and PGA2 further enhanced the migratory and T-cell-stimulatory capacity of TNF-alpha-treated moDCs. Dinoprostone 5-9 tumor necrosis factor Homo sapiens 85-94 15676206-8 2005 Maturation of moDCs with either PGE2 or PGA2 resulted in enhanced IFN-gamma, TNF-alpha, and IL-5 production and repressed IL-10 production in allogeneic mixed leukocyte cultures. Dinoprostone 32-36 tumor necrosis factor Homo sapiens 77-86 15371556-8 2004 In aged monocytes, rolipram, Org 9935 (a PDE3 inhibitor), and prostaglandin E2 inhibited TNFalpha generation in a concentration-dependent manner and interacted additively with BRL 50481. Dinoprostone 62-78 tumor necrosis factor Homo sapiens 89-97 15621371-8 2005 IL-1beta and TNFalpha treatment for 24 h enhanced prostaglandin E2 (PGE2) production 2-4-fold, which was blocked by pretreatment with the COX-2 inhibitor, NS-398. Dinoprostone 50-66 tumor necrosis factor Homo sapiens 13-21 15621371-8 2005 IL-1beta and TNFalpha treatment for 24 h enhanced prostaglandin E2 (PGE2) production 2-4-fold, which was blocked by pretreatment with the COX-2 inhibitor, NS-398. Dinoprostone 68-72 tumor necrosis factor Homo sapiens 13-21 15642051-6 2005 RESULTS: The cytokine TNFalpha enhanced the expression of mRNA as well as the protein levels of both COX-2 and mPGES-1 and subsequently the production of PGE2 in gingival fibroblasts. Dinoprostone 154-158 tumor necrosis factor Homo sapiens 22-30 15642051-7 2005 Treatment of gingival fibroblasts with triclosan (1 microg/ml) significantly reduced the stimulatory effect of TNFalpha (10 ng/ml) on the expression of mPGES-1 at both the mRNA and the protein level by an average of 21% and 43%, respectively, and subsequently the production of PGE2 (p<0.01). Dinoprostone 278-282 tumor necrosis factor Homo sapiens 111-119 15777610-0 2005 Rolipram, salbutamol and prostaglandin E2 suppress TNFalpha release from human monocytes by activating Type II cAMP-dependent protein kinase. Dinoprostone 25-41 tumor necrosis factor Homo sapiens 51-59 15667901-4 2005 PGE2 and PGF2alpha were the prostanoids released in greatest quantity in response to TNF-alpha. Dinoprostone 0-4 tumor necrosis factor Homo sapiens 85-94 15379866-7 2004 Upon addition of PGE2, however, LPS-induced IL-6 and TNF-alpha production was suppressed regardless of indomethacin presence. Dinoprostone 17-21 tumor necrosis factor Homo sapiens 53-62 15342193-0 2004 Mechanisms involved in prostaglandin E2-mediated neuroprotection against TNF-alpha: possible involvement of multiple signal transduction and beta-catenin/T-cell factor. Dinoprostone 23-39 tumor necrosis factor Homo sapiens 73-82 15342193-3 2004 In a continuation of this work, the present study investigated the direct effect of PGE2, one of the major prostaglandins produced in the brain, on cell viability in SH-SY5Y neuronal cells treated with TNF-alpha. Dinoprostone 84-88 tumor necrosis factor Homo sapiens 202-211 15342193-4 2004 PGE2 did not promote neurotoxicity, but rather had a strong protective effect against TNF-alpha by ameliorating TNF-alpha-induced apoptosis and also by rescuing the intracellular level of beta-catenin, a key transducer of the Wnt signaling pathway. Dinoprostone 0-4 tumor necrosis factor Homo sapiens 86-95 15342193-4 2004 PGE2 did not promote neurotoxicity, but rather had a strong protective effect against TNF-alpha by ameliorating TNF-alpha-induced apoptosis and also by rescuing the intracellular level of beta-catenin, a key transducer of the Wnt signaling pathway. Dinoprostone 0-4 tumor necrosis factor Homo sapiens 112-121 15342193-6 2004 Pharmacological studies provided further evidence supporting the notion that PGE2-mediated neuroprotection against TNF-alpha involves the stimulation of Tcf/Lef signaling through EP1-, EP2-, and EP4-mediated increases of beta-catenin in SH-SY5Y cells. Dinoprostone 77-81 tumor necrosis factor Homo sapiens 115-124 15342193-7 2004 In addition, this PGE2 effect appears to be dependent on the activation of protein kinase A, phosphatidylinositol 3-kinase, phospholipase C, and to a lesser extent protein kinase C. Thus, the molecular mechanism governing the inhibitory effect of PGE2 against TNF-alpha may involve the activation and cross talk of multiple signal transduction and play an important role in regulating the survival of neurons during the neurotoxic inflammatory response associated with neurodegenerative diseases including AD. Dinoprostone 18-22 tumor necrosis factor Homo sapiens 260-269 15501405-0 2004 Implication of prostaglandin E(2) in TNF-alpha-induced release of m-calpain from HCS-2/8 chondrocytes. Dinoprostone 15-33 tumor necrosis factor Homo sapiens 37-46 15464057-2 2004 Exogenous prostaglandin E(2) (IC(50)<5 nM) inhibited endotoxin-induced TNFalpha mRNA and protein while, up to 1 microM, it did not significantly affect cyclooxygenase-2 mRNA expression. Dinoprostone 10-28 tumor necrosis factor Homo sapiens 74-82 15316388-1 2004 Some trauma patients" monocytes (MO) increase TNF-alpha levels concomitant to augmenting production of the TNF-alpha inhibitor prostaglandin E2 (PGE2), suggesting posttrauma MO insensitivity to PGE2 effects. Dinoprostone 127-143 tumor necrosis factor Homo sapiens 107-116 15316388-1 2004 Some trauma patients" monocytes (MO) increase TNF-alpha levels concomitant to augmenting production of the TNF-alpha inhibitor prostaglandin E2 (PGE2), suggesting posttrauma MO insensitivity to PGE2 effects. Dinoprostone 145-149 tumor necrosis factor Homo sapiens 107-116 15316388-5 2004 MO TNF-alpha sensitivity to down-regulation by IL-10 was retained, suggesting that PGE2-related functions are specifically altered in these patients" MO. Dinoprostone 83-87 tumor necrosis factor Homo sapiens 3-12 15229940-12 2004 T cell derived IL-17, especially in combination with TNF-a, may contribute to ongoing inflammation through its effects on COX-2 expression and PGE2 production. Dinoprostone 143-147 tumor necrosis factor Homo sapiens 53-58 15379214-4 2004 The results showed that IL-1beta as well as TNFalpha induced mPGES-1 mRNA and protein expression accompanied by enhanced PGE2 production in gingival fibroblasts. Dinoprostone 121-125 tumor necrosis factor Homo sapiens 44-52 14751545-1 2004 This study was to determine the mechanism of tumor necrosis factor-alpha (TNF-alpha)-enhanced cyclooxygenase (COX)-2 expression associated with prostaglandin E2 (PGE2) synthesis in human tracheal smooth muscle cells (HTSMCs). Dinoprostone 144-160 tumor necrosis factor Homo sapiens 45-72 14751545-1 2004 This study was to determine the mechanism of tumor necrosis factor-alpha (TNF-alpha)-enhanced cyclooxygenase (COX)-2 expression associated with prostaglandin E2 (PGE2) synthesis in human tracheal smooth muscle cells (HTSMCs). Dinoprostone 144-160 tumor necrosis factor Homo sapiens 74-83 14751545-1 2004 This study was to determine the mechanism of tumor necrosis factor-alpha (TNF-alpha)-enhanced cyclooxygenase (COX)-2 expression associated with prostaglandin E2 (PGE2) synthesis in human tracheal smooth muscle cells (HTSMCs). Dinoprostone 162-166 tumor necrosis factor Homo sapiens 45-72 14751545-1 2004 This study was to determine the mechanism of tumor necrosis factor-alpha (TNF-alpha)-enhanced cyclooxygenase (COX)-2 expression associated with prostaglandin E2 (PGE2) synthesis in human tracheal smooth muscle cells (HTSMCs). Dinoprostone 162-166 tumor necrosis factor Homo sapiens 74-83 14751545-2 2004 TNF-alpha markedly increased COX-2 expression and PGE2 synthesis in a time- and concentration-dependent manner, whereas COX-1 remained unaltered. Dinoprostone 50-54 tumor necrosis factor Homo sapiens 0-9 14751545-3 2004 Tyrosine kinase inhibitor (genistein), phosphatidylcholine-specific phospholipase C (PC-PLC) inhibitor (D-609) and PKC inhibitor (GF109203X) attenuated TNF-alpha-induced COX-2 expression and PGE2 synthesis in HTSMCs. Dinoprostone 191-195 tumor necrosis factor Homo sapiens 152-161 14751545-4 2004 TNF-alpha-induced COX-2 expression and PGE2 synthesis were also inhibited by PD98059 (an inhibitor of MEK1/2) and SB203580 and SB202190 (inhibitors of p38 MAPK), respectively, suggesting the involvement of p42/p44 and p38 MAPKs in these responses. Dinoprostone 39-43 tumor necrosis factor Homo sapiens 0-9 15023855-4 2004 TNF alpha induced concentration- and time-dependent upregulation of COX-2 mRNA, protein and prostaglandin (PG)E(2) synthesis. Dinoprostone 92-114 tumor necrosis factor Homo sapiens 0-9 15023855-10 2004 TNF alpha-induced PGE(2) biosynthesis was significantly enhanced by the simultaneous addition of IFN gamma and was COX-2 dependent. Dinoprostone 18-24 tumor necrosis factor Homo sapiens 0-9 15379214-2 2004 Previously we have reported that the inflammatory mediators interleukin-1beta, (IL-1beta) and tumor necrosis factor alpha (TNFalpha) stimulate PGE2 synthesis by inducing mRNA expression of cyclooxygenase-2 (COX-2) in human gingival fibroblasts. Dinoprostone 143-147 tumor necrosis factor Homo sapiens 94-121 15379214-2 2004 Previously we have reported that the inflammatory mediators interleukin-1beta, (IL-1beta) and tumor necrosis factor alpha (TNFalpha) stimulate PGE2 synthesis by inducing mRNA expression of cyclooxygenase-2 (COX-2) in human gingival fibroblasts. Dinoprostone 143-147 tumor necrosis factor Homo sapiens 123-131 14872092-1 2004 Prostaglandin (PG) E(2) induces dendritic cell maturation in cooperation with proinflammatory cytokines [such as tumor necrosis factor (TNF)-alpha and interleukin (IL)-1beta]. Dinoprostone 0-23 tumor necrosis factor Homo sapiens 113-146 14751545-8 2004 These findings suggest that the increased expression of COX-2 correlates with the release of PGE2 from TNF-alpha-challenged HTSMCs, at least in part, mediated through p42/p44 and p38 MAPKs as well as NF-kappaB signaling pathways in HTSMCs. Dinoprostone 93-97 tumor necrosis factor Homo sapiens 103-112 15134897-5 2004 In addition, TNF-alpha alone stimulated the elaboration of KC, MIP-2, PGE2 and VEGF in fibroblasts. Dinoprostone 70-74 tumor necrosis factor Homo sapiens 13-22 15134897-8 2004 These results indicate that IL-17 up-regulates elaboration of various proangiogenic factors, and modulates macrophage-derived TNF-alpha-induced production of KC, MIP-2, PGE2 and VEGF by fibroblasts. Dinoprostone 169-173 tumor necrosis factor Homo sapiens 126-135 15219461-0 2004 Inhibition of IL-6, TNF-alpha, and cyclooxygenase-2 protein expression by prostaglandin E2-induced IL-10 in bone marrow-derived dendritic cells. Dinoprostone 74-90 tumor necrosis factor Homo sapiens 20-29 15379214-5 2004 The anti-inflammatory steroid dexamethasone (DEX) inhibited mPGES-1 mRNA and protein expression as well as PGE2 production induced by IL-1beta or TNFalpha. Dinoprostone 107-111 tumor necrosis factor Homo sapiens 146-154 15379214-7 2004 The results demonstrate that mPGES-1 regulates PGE2 production in gingival fibroblasts stimulated by inflammatory mediators IL-1beta and TNFa. Dinoprostone 47-51 tumor necrosis factor Homo sapiens 137-141 12349897-10 2002 PDTC and herbimycin A attenuated TNF-alpha-stimulated PGE2 release. Dinoprostone 54-58 tumor necrosis factor Homo sapiens 33-42 15373964-10 2004 Since fever induced by IL-1, TNF-alpha, IL-6 or TLR ligands requires cyclooxygenase-2, production of prostaglandin E2 (PGE2) and activation of hypothalamic PGE2 receptors provides a unifying mechanism for fever by endogenous and exogenous pyrogens. Dinoprostone 101-117 tumor necrosis factor Homo sapiens 29-38 15201939-3 2004 IL-1 is considered a key mediator in RA joint damage because of its greater capacity (greater than TNF) of increasing matrix degradation by inducing the production of MMPs and PGE2 in synovial cells, as well by its role as mediator of bone and cartilage destruction. Dinoprostone 176-180 tumor necrosis factor Homo sapiens 99-102 14632643-3 2003 Prostaglandin E2 (PGE2), a proinflammatory mediator supporting dendritic cell activation and necessary for adequate DC migration, leads to the up-regulation of C5aR expression when incubated alone and prevents down-regulation when given in combination with TNF-alpha or LPS. Dinoprostone 0-16 tumor necrosis factor Homo sapiens 257-266 14632643-3 2003 Prostaglandin E2 (PGE2), a proinflammatory mediator supporting dendritic cell activation and necessary for adequate DC migration, leads to the up-regulation of C5aR expression when incubated alone and prevents down-regulation when given in combination with TNF-alpha or LPS. Dinoprostone 18-22 tumor necrosis factor Homo sapiens 257-266 12970750-4 2003 Here we demonstrate that the selective COX-2 inhibitors NS-398 and nimesulide increased TNF sensitivity of TNF-resistant HeLa H21 and TNF-sensitive HeLa D98 cells, although this cytokine induced significant COX-2 activity, as judged by prostaglandin E(2) (PGE(2)) production, only in H21 cells. Dinoprostone 236-254 tumor necrosis factor Homo sapiens 107-110 12970750-4 2003 Here we demonstrate that the selective COX-2 inhibitors NS-398 and nimesulide increased TNF sensitivity of TNF-resistant HeLa H21 and TNF-sensitive HeLa D98 cells, although this cytokine induced significant COX-2 activity, as judged by prostaglandin E(2) (PGE(2)) production, only in H21 cells. Dinoprostone 236-254 tumor necrosis factor Homo sapiens 107-110 15067740-12 2004 CONCLUSION: TP could significantly down-regulate TNFalpha-induced COX-2, iNOS expression and production of PGE2, NO in human RASF, which is associated with the suppression of NF-kappaB activity. Dinoprostone 107-111 tumor necrosis factor Homo sapiens 49-57 15225371-12 2004 In comparison with 6-keto-PGF1alpha and thromboxane B2, the production of PGE2 was greater after chondrocytes were stimulated by IL-1beta or TNF-alpha. Dinoprostone 74-78 tumor necrosis factor Homo sapiens 141-150 15373964-10 2004 Since fever induced by IL-1, TNF-alpha, IL-6 or TLR ligands requires cyclooxygenase-2, production of prostaglandin E2 (PGE2) and activation of hypothalamic PGE2 receptors provides a unifying mechanism for fever by endogenous and exogenous pyrogens. Dinoprostone 119-123 tumor necrosis factor Homo sapiens 29-38 12958688-7 2003 Anti-estrogen (ICI 164,384) inclusion prevented the estrogen-dependent increase in PGE2 production in the TGFbeta plus TNF-stimulated samples. Dinoprostone 83-87 tumor necrosis factor Homo sapiens 119-122 12874281-9 2003 Hypoxia also increased TNF-alpha synthesis, which appeared to play a role in COX-2 expression, and the observed increase TNF-alpha synthesis appeared to result from reduced PGE2 synthesis. Dinoprostone 173-177 tumor necrosis factor Homo sapiens 121-130 12496396-0 2003 Critical paracrine interactions between TNF-alpha and IL-10 regulate lipopolysaccharide-stimulated human choriodecidual cytokine and prostaglandin E2 production. Dinoprostone 133-149 tumor necrosis factor Homo sapiens 40-49 12496396-7 2003 Immunoneutralization studies indicated that TNF-alpha was a primary regulator of IL-1beta, IL-10, and PGE2 production, while IL-1beta stimulated only PGE2 production. Dinoprostone 102-106 tumor necrosis factor Homo sapiens 44-53 12452446-4 2002 Moreover, TNFalpha, which also stimulates aromatase expression in breast adipose stromal cells, acts to increase the secretion of PGE2 by these cells, as well as the expression of COX 2 and PGE synthase, but not that of COX 1. Dinoprostone 130-134 tumor necrosis factor Homo sapiens 10-18 12349897-0 2002 Tumor necrosis factor alpha (TNF-alpha)-induced prostaglandin E2 release is mediated by the activation of cyclooxygenase-2 (COX-2) transcription via NFkappaB in human gingival fibroblasts. Dinoprostone 48-64 tumor necrosis factor Homo sapiens 0-27 12349897-0 2002 Tumor necrosis factor alpha (TNF-alpha)-induced prostaglandin E2 release is mediated by the activation of cyclooxygenase-2 (COX-2) transcription via NFkappaB in human gingival fibroblasts. Dinoprostone 48-64 tumor necrosis factor Homo sapiens 29-38 12349897-5 2002 In this paper, we investigated the involvement of NFkappaB on TNF-alpha-mediated prostaglandin E2 (PGE2) release and COX-2 gene expression in human gingival fibroblasts (HGF). Dinoprostone 81-97 tumor necrosis factor Homo sapiens 62-71 12349897-5 2002 In this paper, we investigated the involvement of NFkappaB on TNF-alpha-mediated prostaglandin E2 (PGE2) release and COX-2 gene expression in human gingival fibroblasts (HGF). Dinoprostone 99-103 tumor necrosis factor Homo sapiens 62-71 12349897-6 2002 TNF-alpha-induced PGE2 release and COX-2 mRNA accumulation in a time- and concentration-dependent manner in HGF. Dinoprostone 18-22 tumor necrosis factor Homo sapiens 0-9 12349897-11 2002 These results suggest that NFkappaB transcription factor is a key regulator of COX-2 expression in TNF-alpha-induced PGE2 production, which is mediated through a tyrosine kinase pathway in HGF. Dinoprostone 117-121 tumor necrosis factor Homo sapiens 99-108 11821123-4 2002 The PLAA peptide and melittin increased the expression of genes encoding the proinflammatory cytokine tumor necrosis factor alpha (TNFalpha) and cyclooxygenase-2 (COX-2), which is involved in PGE(2) production. Dinoprostone 192-198 tumor necrosis factor Homo sapiens 102-129 12113550-8 2002 These findings indicate that prostaglandin E2 has a lowering effect on TNFalpha-enhanced MMP-13 mRNA levels, and that this effect is dependent on cAMP. Dinoprostone 29-45 tumor necrosis factor Homo sapiens 71-79 12113550-9 2002 Our results suggest that TNFalpha participates in periodontal ligament destruction by stimulating the production of MMPs (MMP-1, MMP-3 and MMP-13), while endogenous prostaglandin E2 has a negative feedback role in TNFalpha-enhanced MMP-13 production. Dinoprostone 165-181 tumor necrosis factor Homo sapiens 214-222 11821123-4 2002 The PLAA peptide and melittin increased the expression of genes encoding the proinflammatory cytokine tumor necrosis factor alpha (TNFalpha) and cyclooxygenase-2 (COX-2), which is involved in PGE(2) production. Dinoprostone 192-198 tumor necrosis factor Homo sapiens 131-139 11875501-7 2002 Inhibition of matrix metalloproteinases (MMPs), transforming growth factor-alpha (TGF-alpha) or c-Src blocked PGE2-mediated EGFR transactivation and downstream signaling indicating that PGE2-induced EGFR transactivation involves signaling transduced via TGF-alpha, an EGFR ligand, likely released by c-Src-activated MMP(s). Dinoprostone 110-114 tumor necrosis factor Homo sapiens 48-80 11875501-7 2002 Inhibition of matrix metalloproteinases (MMPs), transforming growth factor-alpha (TGF-alpha) or c-Src blocked PGE2-mediated EGFR transactivation and downstream signaling indicating that PGE2-induced EGFR transactivation involves signaling transduced via TGF-alpha, an EGFR ligand, likely released by c-Src-activated MMP(s). Dinoprostone 186-190 tumor necrosis factor Homo sapiens 48-80 11879548-3 2002 In combination with TNF or IL-1beta, hTWEAK further stimulated the secretion of prostaglandin E2, MMP-1, IL-6 and IL-8 up to fourfold, and IP-10 and RANTES up to 70-fold compared to TNF or IL-1beta alone. Dinoprostone 80-96 tumor necrosis factor Homo sapiens 20-23 11821061-2 2002 Prostaglandin E2 (PGE2), which is a member of the eicosanoid family of oxygenated arachidonic acid derivatives generated through the action of cyclooxygenases (COXs), is frequently used to enhance the tumor necrosis factor-alpha-induced terminal maturation of moDCs. Dinoprostone 0-16 tumor necrosis factor Homo sapiens 201-228 11821061-2 2002 Prostaglandin E2 (PGE2), which is a member of the eicosanoid family of oxygenated arachidonic acid derivatives generated through the action of cyclooxygenases (COXs), is frequently used to enhance the tumor necrosis factor-alpha-induced terminal maturation of moDCs. Dinoprostone 18-22 tumor necrosis factor Homo sapiens 201-228 11739553-3 2001 In a dose-dependent manner, 8-Bromo cAMP, prostaglandin E(2), and 3-isobutyl-1-methylxanthine inhibited tumor necrosis factor alpha release and suppressed antigen presentation by DCs. Dinoprostone 42-60 tumor necrosis factor Homo sapiens 104-131 12219935-6 2002 Finally, the effects of hTNF-alpha on bovine granulosa cells are not mediated by nitric oxide or cAMP, as neither of these substances were affected by treatment with the cytokine; however, in some way, they could be mediated through PGE2 and PGF2alpha, the production of which was inhibited by TNF-alpha in cells from small follicles. Dinoprostone 233-237 tumor necrosis factor Homo sapiens 24-34