PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 20498218-11 2010 Experimental increase of cytoplasmic catecholamines by VMAT2 blockade strongly reduced tumour necrosis factor (TNF) independently of canonical extracellular beta-adrenergic signalling. Catecholamines 37-51 tumor necrosis factor Homo sapiens 87-109 20044210-4 2010 Catecholamines and cortisol in plasma and lipopolysaccharide (LPS) stimulated levels of TNF-alpha and IL-6 by peripheral leucocytes were assessed along with severity of obsessive-compulsive symptoms, disgust, and anxiety levels using Visual Analogue Scales prior, during and after a provocation paradigm. Catecholamines 0-14 tumor necrosis factor Homo sapiens 88-97 20498218-11 2010 Experimental increase of cytoplasmic catecholamines by VMAT2 blockade strongly reduced tumour necrosis factor (TNF) independently of canonical extracellular beta-adrenergic signalling. Catecholamines 37-51 tumor necrosis factor Homo sapiens 111-114 18649956-5 2009 Since it is well known that myocardial damage caused by catecholamines can induce synthesis of cytokines by myocytes, cytokines, specifically those with known cardiodepressant properties such as TNF-alpha, could be an alternative mechanism involved in cardiac dysfunction in the setting of tetanus. Catecholamines 56-70 tumor necrosis factor Homo sapiens 195-204 18669662-8 2008 Surgical ablation of the splenic nerve and catecholamine depletion by reserpine indicate that these nerves are catecholaminergic and are required for functional inhibition of TNF production by vagus nerve stimulation. Catecholamines 43-56 tumor necrosis factor Homo sapiens 175-178 12511144-12 2003 Despite significantly more fluid and catecholamine administration in the TNF group, the mean arterial pressure and the systemic vascular resistance index were significantly (P<.001) lower than in the non-TNF group. Catecholamines 37-50 tumor necrosis factor Homo sapiens 73-76 18234565-2 2008 The aim of this study was to determine the effect of exogenous catecholamines on tumor necrosis factor alpha (TNFa), interleukin-6 (IL-6), interleukin-10 (IL-10) and beta(beta)-endorphin levels in patients with severe trauma, during the first 24 h after injury. Catecholamines 63-77 tumor necrosis factor Homo sapiens 81-108 18234565-6 2008 Baseline values were different between the two groups, but an altered pattern of release was observed for TNFa, IL-6, IL-10 and beta-endorphin levels in patients treated with catecholamines. Catecholamines 175-189 tumor necrosis factor Homo sapiens 106-110 16855135-2 2006 Recent evidence indicates that glucocorticoids (GCs) and catecholamines (CAs), the major stress hormones, inhibit systemically IL-12, TNF-alpha, and INF-gamma, but upregulate IL-10, IL-4, and TGF-beta production. Catecholamines 57-71 tumor necrosis factor Homo sapiens 134-143 16855135-2 2006 Recent evidence indicates that glucocorticoids (GCs) and catecholamines (CAs), the major stress hormones, inhibit systemically IL-12, TNF-alpha, and INF-gamma, but upregulate IL-10, IL-4, and TGF-beta production. Catecholamines 73-76 tumor necrosis factor Homo sapiens 134-143 16889669-6 2006 Catecholamines inhibited the synthesis of IFN-gamma, TNF-alpha, and IL-10 at a concentration of 10(-5) M. In addition, IFN-gamma release was suppressed by 10(-7) M epinephrine. Catecholamines 0-14 tumor necrosis factor Homo sapiens 53-62 19091080-2 2008 In septic shock, endogenous catecholamines induce beta2-AR downregulation, leading to an increased TNF-alpha release. Catecholamines 28-42 tumor necrosis factor Homo sapiens 99-108 16985181-3 2007 Catecholamine release results in reduced production of interleukin-10 and transforming growth factor-beta by Tregs, and in down-regulation of Treg-dependent inhibition of effector T-lymphocyte (Teff) proliferation, which occurs without affecting the production of tumor necrosis factor-alpha or interferon-gamma. Catecholamines 0-13 tumor necrosis factor Homo sapiens 264-291 15145612-1 2004 Endogenous catecholamine, epinephrine and norepinephrine, and isoproterenol concentration-dependently induced the production of interleukin (IL)-18, tumor necrosis factor (TNF)-alpha and interferon (IFN)-gamma, and inhibited that of IL-10 in human peripheral blood mononuclear cells (PBMC). Catecholamines 11-24 tumor necrosis factor Homo sapiens 149-182 14685702-3 2004 Physiological dampeners of TNFalpha production, such as interleukin-10, catecholamines, cortisol, and others fail in the course of the disease. Catecholamines 72-86 tumor necrosis factor Homo sapiens 27-35 12151739-3 2002 The influence of catecholamine pretreatment on tumor necrosis factor (TNF)-alpha-mediated production of these chemokines and the expression of adhesion molecules was also tested. Catecholamines 17-30 tumor necrosis factor Homo sapiens 47-80 10823386-3 2000 MAIN RESULTS: Catecholamines (epinephrine, norepinephrine, isoproterenol, and dopamine) in general inhibit tumor necrosis factor-alpha (TNF) production and may enhance interleukin-6 (IL-6) and IL-10 production. Catecholamines 14-28 tumor necrosis factor Homo sapiens 107-134 11782970-10 2002 This finding reveals a role for endogenous catecholamines in the regulation of TNF production. Catecholamines 43-57 tumor necrosis factor Homo sapiens 79-82 12114286-1 2002 Recent evidence indicates that glucocorticoids and catecholamines, the major stress hormones, inhibit the production of proinflammatory cytokines, such as interleukin (IL)-12, tumor necrosis factor (TNF)-alpha, and interferon (IFN)-gamma, whereas they stimulate the production of antiinflammatory cytokines, such as IL-10, IL-4, and transforming growth factor (TGF)-beta. Catecholamines 51-65 tumor necrosis factor Homo sapiens 176-209 11084220-1 2000 There are some reports that catecholamines may modulate the production of monocytic cytokines such as interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF alpha). Catecholamines 28-42 tumor necrosis factor Homo sapiens 127-154 11084220-1 2000 There are some reports that catecholamines may modulate the production of monocytic cytokines such as interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF alpha). Catecholamines 28-42 tumor necrosis factor Homo sapiens 156-165 10823386-3 2000 MAIN RESULTS: Catecholamines (epinephrine, norepinephrine, isoproterenol, and dopamine) in general inhibit tumor necrosis factor-alpha (TNF) production and may enhance interleukin-6 (IL-6) and IL-10 production. Catecholamines 14-28 tumor necrosis factor Homo sapiens 136-139 9435537-0 1997 Catecholamines increase monocyte TNF receptors and inhibit TNF through beta 2-adrenoreceptor activation. Catecholamines 0-14 tumor necrosis factor Homo sapiens 33-36 10588509-1 1999 Studies performed on healthy volunteers have revealed that catecholamines down-regulate the lipopolysaccharide (LPS)-induced production of tumor necrosis factor (TNF)alpha, interleukin (IL)-6, and IL-1beta. Catecholamines 59-73 tumor necrosis factor Homo sapiens 139-160 10588509-1 1999 Studies performed on healthy volunteers have revealed that catecholamines down-regulate the lipopolysaccharide (LPS)-induced production of tumor necrosis factor (TNF)alpha, interleukin (IL)-6, and IL-1beta. Catecholamines 59-73 tumor necrosis factor Homo sapiens 162-171 10588509-7 1999 Correspondingly, in blood of patients with prolonged severe sepsis, TNFalpha was reduced by 67.2% (P < 0.0001) and IL-6 was reduced by 32.9% (P < 0.0001); IL-1beta and IL-10 were not modulated by catecholamines in these patients. Catecholamines 202-216 tumor necrosis factor Homo sapiens 68-76 9435537-0 1997 Catecholamines increase monocyte TNF receptors and inhibit TNF through beta 2-adrenoreceptor activation. Catecholamines 0-14 tumor necrosis factor Homo sapiens 59-62 9435537-3 1997 Also, catecholamines inhibit TNF production, but the adrenoreceptor mechanism of this effect has not been fully clarified. Catecholamines 6-20 tumor necrosis factor Homo sapiens 29-32 8982123-2 1996 In healthy individuals, catecholamines can inhibit the production of pro-inflammatory cytokines like interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-alpha) via interaction with beta 2-adrenergic receptors. Catecholamines 24-38 tumor necrosis factor Homo sapiens 126-153 8982123-2 1996 In healthy individuals, catecholamines can inhibit the production of pro-inflammatory cytokines like interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-alpha) via interaction with beta 2-adrenergic receptors. Catecholamines 24-38 tumor necrosis factor Homo sapiens 155-164 1737985-0 1992 Tumor necrosis factor modulates the inactivation of catecholamine secretion in cultured sympathetic neurons. Catecholamines 52-65 tumor necrosis factor Homo sapiens 0-21 30933434-0 2019 TNF-alpha Upregulates IKKepsilon Expression via the Lin28B/let-7a Pathway to Induce Catecholamine Resistance in Adipocytes. Catecholamines 84-97 tumor necrosis factor Homo sapiens 0-9 30933434-13 2019 TNF-alpha induces catecholamine resistance via activation of the Lin28B/let-7a/IKKepsilon pathway. Catecholamines 18-31 tumor necrosis factor Homo sapiens 0-9 28011264-3 2017 We investigated the effects of 20-min moderate (65-70% VO2 peak) exercise-induced catecholamine production on LPS-stimulated TNF production by monocytes in 47 healthy volunteers and determined AR subtypes involved. Catecholamines 82-95 tumor necrosis factor Homo sapiens 125-128 29941879-0 2018 TNF inhibits catecholamine production from induced sympathetic neuron-like cells in rheumatoid arthritis and osteoarthritis in vitro. Catecholamines 13-26 tumor necrosis factor Homo sapiens 0-3 29941879-8 2018 In mixed synovial cells, significant effects of TNF on catecholamine release were observed only in OA. Catecholamines 55-68 tumor necrosis factor Homo sapiens 48-51