PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 17763411-0 2007 Pattern of interleukin-1beta secretion in response to lipopolysaccharide and ATP before and after interleukin-1 blockade in patients with CIAS1 mutations. Adenosine Triphosphate 77-80 interleukin 1 alpha Homo sapiens 11-24 19748989-2 2009 Accruing evidence suggests that extracellular ATP participates in the inflammatory response as a proinflammatory mediator by activating the inflammasome complex, inducing secretion of cytokines (IL-1, IL-18) and cell damaging agents such as oxygen radicals, cationic proteins, and metalloproteases. Adenosine Triphosphate 46-49 interleukin 1 alpha Homo sapiens 195-199 19542372-5 2009 In addition to TNF-alpha, IL-1alpha and IL-1beta promoted caspase-1 activation via Nlrp3 in response to ATP. Adenosine Triphosphate 104-107 interleukin 1 alpha Homo sapiens 26-35 14741428-4 2004 BzATP induction of IL-1alpha and IL-1beta secretion from microglia was completely reversed by pre-incubation of the cells with the P2X7 antagonist, adenosine 5"-triphosphate 2",3"-acyclic dialcohol (oxidized ATP). Adenosine Triphosphate 2-5 interleukin 1 alpha Homo sapiens 19-28 16512913-12 2006 CONCLUSION: It is hypothesized that the known increase of lesion-associated extracellular ATP contributes via P2X7 activation to release IL-1 beta which in turn induces COX-2 and downstream pathogenic mediators. Adenosine Triphosphate 90-93 interleukin 1 alpha Homo sapiens 137-146 12151017-7 2002 This review discusses the potential involvement of extracellular ATP and P2X7 receptors as regulators of interleukin-1-mediated neuropathologies and thus as a mediator of cell death following pathological insults. Adenosine Triphosphate 65-68 interleukin 1 alpha Homo sapiens 105-118 10733939-2 2000 Interleukin-1 (IL-1) beta release from Mφ in response to LPS, appears to be mediated by the autocrine/paracrine release of ATP via P2X7 receptor activation. Adenosine Triphosphate 131-134 interleukin 1 alpha Homo sapiens 0-13 11160202-5 2001 On the other hand, ATP markedly and dose-dependently inhibited LPS- and soluble CD40 ligand-dependent production of IL-1alpha, IL-1beta, TNF-alpha, IL-6, and IL-12, whereas IL-1 receptor antagonist and IL-10 production was not affected. Adenosine Triphosphate 19-22 interleukin 1 alpha Homo sapiens 116-125 10733939-4 2000 To determine whether CD39 modulates ATP-mediated release of IL-1 from EC, we stimulated human EC with LPS and measured levels of ATP secretion and IL-1 release. Adenosine Triphosphate 36-39 interleukin 1 alpha Homo sapiens 60-64 10733939-5 2000 LPS triggered ATP secretion from EC that was soon followed by IL-1alpha release. Adenosine Triphosphate 14-17 interleukin 1 alpha Homo sapiens 62-71 9485082-6 1998 ATP and UTP stimulated a small, but significant, increase in PG release from resting synoviocytes and a dramatic increase in PG release from synoviocytes prestimulated with recombinant human IL-1alpha. Adenosine Triphosphate 0-3 interleukin 1 alpha Homo sapiens 191-200 9376221-5 1997 These MAP kinase homologues are integral components of parallel MAP kinase cascades activated in response to a number of cellular stresses including inflammatory cytokines (e.g., Interleukin-1 (Il-1) and tumour necrosis factor-alpha (TNF-alpha), heat and chemical shock, bacterial endotoxin and ischaemia/cellular ATP depletion. Adenosine Triphosphate 314-317 interleukin 1 alpha Homo sapiens 179-198 9271402-6 1997 We identified a putative NLS in the G-kinase ATP binding domain which resembles the NLS of the interleukin-1alpha precursor. Adenosine Triphosphate 45-48 interleukin 1 alpha Homo sapiens 95-113 34066647-5 2021 Our results indicated that ethyl pyruvate significantly suppressed LPS and ATP-induced NLRP3 inflammasome activation, decreased active caspase-1 level, secretion of IL-1beta and IL-18 cytokines, and reduced the level of pyroptotic cell death resulting from inflammasome activation. Adenosine Triphosphate 75-78 interleukin 1 alpha Homo sapiens 165-173 34075628-14 2021 (viii) Stimulation of P2X7 receptors by ATP induced IL-1beta in ear-pinnas. Adenosine Triphosphate 40-43 interleukin 1 alpha Homo sapiens 52-60 34075628-16 2021 These results suggest that (1) N-BPs induce both early- and late-phase inflammation via ATP-production and P2X7-receptor stimulation, (2) N-BPs and LPS induce mutually augmenting responses both early and late phases via ATP-mediated IL-1beta production by neutrophils, macrophages, and/or dendritic cells, and (3) NET production by IL-1beta-stimulated neutrophils may mediate the late phase, leading to prolonged inflammation. Adenosine Triphosphate 88-91 interleukin 1 alpha Homo sapiens 332-340 34075628-16 2021 These results suggest that (1) N-BPs induce both early- and late-phase inflammation via ATP-production and P2X7-receptor stimulation, (2) N-BPs and LPS induce mutually augmenting responses both early and late phases via ATP-mediated IL-1beta production by neutrophils, macrophages, and/or dendritic cells, and (3) NET production by IL-1beta-stimulated neutrophils may mediate the late phase, leading to prolonged inflammation. Adenosine Triphosphate 220-223 interleukin 1 alpha Homo sapiens 233-241 33774155-8 2021 As anti-inflammatory functions of AAT are of increasing clinical interest, we compared the potential of two widely used AAT preparations, Prolastin and Respreeza , to inhibit the ATP-induced release of IL-1beta using human monocytic U937 cells. Adenosine Triphosphate 180-183 interleukin 1 alpha Homo sapiens 203-211 33774155-10 2021 The AAT preparation Respreeza is less active compared to Prolastin regarding the inhibition of the ATP-induced release of monocytic IL-1beta. Adenosine Triphosphate 101-104 interleukin 1 alpha Homo sapiens 134-142 34606909-4 2021 LPS induced-tissue damage promotes an elevation of extracellular ATP, triggering the NRLP3-inflammasome assembly and activation that, sequentially, induces caspase-1 cleavage and IL-1beta processing and secretion. Adenosine Triphosphate 65-68 interleukin 1 alpha Homo sapiens 179-187 34452455-7 2021 When the models were challenged with a combination of the bacterial toxins LPS and ATP, a release of the proinflammatory cytokines IL-1beta and IL-8 was observed, confirming that the model can generate an immune response. Adenosine Triphosphate 83-86 interleukin 1 alpha Homo sapiens 131-139 34377468-7 2021 Oxidised forms of these lipoproteins reduced the secretion of mature IL-1beta also by inhibiting the activation of NLRP3 inflammasome induced by SAA, ATP, nigericin and monosodium urate crystals. Adenosine Triphosphate 150-153 interleukin 1 alpha Homo sapiens 69-77 34209843-3 2021 The obtained compounds were screened in vitro to test their ability to inhibit NLRP3-dependent pyroptosis and IL-1beta release in PMA-differentiated THP-1 cells stimulated with LPS/ATP. Adenosine Triphosphate 181-184 interleukin 1 alpha Homo sapiens 110-118 34209843-5 2021 From this screening, compounds 9, 13 and 18, able to concentration-dependently inhibit IL-1beta release in LPS/ATP-stimulated human macrophages, emerged as the most promising NLRP3 inhibitors of the series. Adenosine Triphosphate 111-114 interleukin 1 alpha Homo sapiens 87-95 35618202-3 2022 We demonstrate a new function of the anionic phospholipids POPG, DOPG, and PIP2 as inhibitors of IL-1beta release by LPS and ATP-induced inflammasome activation in human monocyte-derived and lung macrophages. Adenosine Triphosphate 125-128 interleukin 1 alpha Homo sapiens 97-105 35563697-8 2022 Our results revealed that CBD and, for the first time, THC significantly inhibited NLRP3 inflammasome activation following LPS + ATP stimulation, leading to a reduction in the levels of IL-1beta in THP-1 macrophages and HBECs. Adenosine Triphosphate 129-132 interleukin 1 alpha Homo sapiens 186-194 34052623-5 2021 In this study, we found that PRV infection caused significant secretion of several pro-inflammatory cytokines in macrophages and promoted IL-1beta secretion in an ATP-dependent manner. Adenosine Triphosphate 163-166 interleukin 1 alpha Homo sapiens 138-146 35443035-7 2022 Moreover, ATP and ADP were significantly positively correlated with the Positive and Negative Symptom Scale (PANSS) item "lack of judgment and insight"; IL-1beta, IL-12 and TNF-alpha were significantly positively correlated with "tension" and "depression"; and "disorientation" and "poor attention" were correlated significantly with IL-6 and IL-8. Adenosine Triphosphate 10-13 interleukin 1 alpha Homo sapiens 153-161 35021019-2 2022 Adenosine-5"-Triphosphate (ATP) triggers interleukin (IL)-1beta secretion via the P2X7 receptor (P2X7R) and activation of the NLRP3 (NOD-, LRR-, and pyrin domain-containing protein 3) inflammasome. Adenosine Triphosphate 27-30 interleukin 1 alpha Homo sapiens 41-63 35431807-6 2022 The ATP-mediated release of IL-1beta by LPS-primed human peripheral blood mononuclear leukocytes, monocytic THP-1 cells and THP-1-derived M1-like macrophages was reduced by both phosphocholine and femtomolar concentrations of pCF3-diEPP. Adenosine Triphosphate 4-7 interleukin 1 alpha Homo sapiens 28-36 35431807-12 2022 However, both agonists signal via nAChR subunits alpha7, alpha9 and/or alpha10 to efficiently down-modulate the ATP-induced release of IL-1beta. Adenosine Triphosphate 112-115 interleukin 1 alpha Homo sapiens 135-143 35236262-5 2022 The co-activation of toll-like receptors 4 (TLR4) by lipopolysaccharide, a constituent of the cell membrane of gram negative bacteria, and the P2X7R by ATP leads to the generation and release of the pro-inflammatory cytokines interleukin-1beta (IL-1beta), IL-6, and tumor necrosis factor-alpha. Adenosine Triphosphate 152-155 interleukin 1 alpha Homo sapiens 245-253 35315432-3 2022 Mechanistically, Panx1 on endothelial cells acts as a conduit for ATP release that stimulates macrophage activation via P2X7 receptors and mitochondrial DNA release to increase IL-1beta and HMGB1 secretion. Adenosine Triphosphate 66-69 interleukin 1 alpha Homo sapiens 177-185 35213000-7 2022 Next, to investigate the crosstalks between KCs and hepatocytes in the context of inflammasome activation, isolated KCs were activated with lipopolysaccharide (LPS), alone or in tandem with ATP, which resulted in inflammasome activation in KCs evident by abundant IL-1beta secretion. Adenosine Triphosphate 190-193 interleukin 1 alpha Homo sapiens 264-272 34052623-6 2021 Furthermore, the expression of IL-1beta can be induced by only PRV infection and depended on NF-kappaB pathway activation, while the subsequent secretion of IL-1beta was mediated by ATP-induced P2 x 7R activation, loss of intracellular K+, and the subsequent NLRP3 inflammasome activation. Adenosine Triphosphate 182-185 interleukin 1 alpha Homo sapiens 157-165 33889075-4 2021 The available data indicates that ATP and glutamate can induce the release of pro inflammatory factors TNF (tumor necrosis factor), IL-1beta (interleukin 1 beta), and NO (nitric oxide) from microglia. Adenosine Triphosphate 34-37 interleukin 1 alpha Homo sapiens 132-140 34006936-7 2021 Addition of ATP to cells following ceramic treatment significantly increased IL-1beta secretion. Adenosine Triphosphate 12-15 interleukin 1 alpha Homo sapiens 77-85 33931497-10 2021 LPS on its own triggered release of TNF-alpha, whereas release of IL-1beta required costimulation by ATP. Adenosine Triphosphate 101-104 interleukin 1 alpha Homo sapiens 66-74 33255431-2 2020 P2X7 receptor (P2X7R) stimulation by extracellular ATP is best known to active the NLRP3 inflammasome and release IL-1beta, but stimulation also leads to release of other cytokines. Adenosine Triphosphate 51-54 interleukin 1 alpha Homo sapiens 114-122 33629290-8 2021 RESULTS: HIF-1alpha and Runx2 were increased, and glucose uptake and ATP generation were decreased in the degenerative CHs from both OA and IL-1beta conditions. Adenosine Triphosphate 69-72 interleukin 1 alpha Homo sapiens 140-148 33471105-5 2021 Leucocyte pore activity was measured by uptake of the fluorescent dye, Yo-Pro-1 and by ATP-induced interleukin (IL)-1beta release. Adenosine Triphosphate 87-90 interleukin 1 alpha Homo sapiens 99-121 33402173-15 2021 Moreover, isoliquiritin protected primary microglia against LPS and adenosine triphosphate (ATP) elicited NLRP3 inflammasome activation in vitro, evidenced by declined protein levels of p-NF-kappaB, NLRP3; cleaved Caspase-1, IL-1beta, and GSDMD-N; upregulated miRNA-27a mRNA expression; and decreased the mRNA and protein levels of SYK. Adenosine Triphosphate 92-95 interleukin 1 alpha Homo sapiens 225-233 32898504-8 2020 Furthermore, we found that Liraglutide protected cardiomyocytes from IL-1beta-induced decreased mitochondrial membrane potential and reduced ATP production. Adenosine Triphosphate 141-144 interleukin 1 alpha Homo sapiens 69-77 32898504-12 2020 Finally, through the study we demonstrated that the blockage of AMPK activity by Compound C abolished the ameliorative effect of Liraglutide on IL-1beta-induced repressed ATP production and triglyceride accumulation, indicating that the action of Liraglutide was dependent on AMPK activation. Adenosine Triphosphate 171-174 interleukin 1 alpha Homo sapiens 144-152 33931964-7 2021 The consequently decreased ATP levels could deactivate NF-kappaB/RelA-IL1alpha pathway, which subsequently results in macrophages reprogrammed to an anti-inflammatory phenotype. Adenosine Triphosphate 27-30 interleukin 1 alpha Homo sapiens 70-78 33524445-2 2021 Niclosamide, CCCP and BAM15 inhibited LPS plus ATP-induced increases of NLRP3 protein and IL-1beta mRNA levels in RAW264.7 macrophages and THP-1 derived macrophages. Adenosine Triphosphate 47-50 interleukin 1 alpha Homo sapiens 90-98 33504771-11 2021 In renal tubular epithelial cells, hypoxia/reoxygenation induced ATP release and extracellular ATP depletion reduced the expression of active IL-1beta. Adenosine Triphosphate 95-98 interleukin 1 alpha Homo sapiens 142-150 33430857-9 2021 Single LPS treatment for chondrocytes downregulated the Col II expression while upregulated the expression of IL-1beta, IL-18, and MMP-13, which was further changed by ATP treatment. Adenosine Triphosphate 168-171 interleukin 1 alpha Homo sapiens 110-118 33430857-12 2021 miR-107 overexpression upregulated the Col II expression while down-regulated the expression of IL-1beta, IL-18, and MMP-13 in supernatant of chondrocytes or chondrocytes induced by LPS and ATP. Adenosine Triphosphate 190-193 interleukin 1 alpha Homo sapiens 96-104 32583615-3 2020 Extracellular ATP contributed to the NLRP3 inflammasome-mediated IL-1beta release, which in turn was preferentially skewed toward Th17 differentiation via enhanced phosphorylation of STAT3. Adenosine Triphosphate 14-17 interleukin 1 alpha Homo sapiens 65-73 32507974-7 2020 RESULTS: LPS-induced inflammation in the presence of ATP activates NLRP3 that subsequently increases pancreatic cancer cell proliferation by increasing caspase-1 activity leading to overall production of IL-1beta. Adenosine Triphosphate 53-56 interleukin 1 alpha Homo sapiens 204-212 33010623-10 2020 Additionally, this analogue exhibited higher potency than BBG at inhibiting the ATP-induced release of IL-1beta in vitro. Adenosine Triphosphate 80-83 interleukin 1 alpha Homo sapiens 103-111 32866784-8 2020 Additionally, IL-1beta/IL-18 secretion from ATP + LPS stimulated THP-1-derived macrophages was RalA-dependently suppressed by levornidazole, suggesting that RalA might have an inhibitory effect on NLRP3 inflammasome activation. Adenosine Triphosphate 44-47 interleukin 1 alpha Homo sapiens 14-22 33152658-6 2020 Treatment of HBCs with both LPS and ATP induced the rapid secretion of high levels of IL-1beta and at the same time, cell death associated with nuclear condensation and cellular swelling. Adenosine Triphosphate 36-39 interleukin 1 alpha Homo sapiens 86-94 33152658-7 2020 HBC treatment with both LPS and ATP induced caspase-1 activation, gasdermin D (GSDMD) cleavage, which mediates pyroptosis, and IL-1beta processing. Adenosine Triphosphate 32-35 interleukin 1 alpha Homo sapiens 127-135 33152658-9 2020 Together, our data indicate that LPS and ATP treatment stimulated NLRP3 inflammasome activation and pyroptosis in HBCs leading to the rapid release of IL-1beta. Adenosine Triphosphate 41-44 interleukin 1 alpha Homo sapiens 151-159 32627113-7 2020 The BzATP and ATP induced calcium overload, mitochondria injury, interleukin-1beta (IL-1beta) secretion, and cytotoxicity can be inhibited by TRPA1 antagonists. Adenosine Triphosphate 6-9 interleukin 1 alpha Homo sapiens 84-92 32035094-7 2020 Treatment with ATP caused the activation of caspase-1 as well as the production of active forms of IL-1beta and IL-18 via P2X7 receptor (P2X7R) in keratinocytes and melanocytes. Adenosine Triphosphate 15-18 interleukin 1 alpha Homo sapiens 99-107 32397236-7 2020 In addition, P2Y2R activation by ATP induced the secretion of IL-1beta and VEGF-A, as well as invasion, in MDA-MB-231 and RT-R-MDA-MB-231 cells, which was inhibited by NLRC4, ASC, and caspase-1 small interfering RNA (siRNA). Adenosine Triphosphate 33-36 interleukin 1 alpha Homo sapiens 62-70 32538272-0 2020 Multi-walled carbon nanotubes induce IL-1beta secretion by activating hemichannels-mediated ATP release in THP-1 macrophages. Adenosine Triphosphate 92-95 interleukin 1 alpha Homo sapiens 37-45 32538272-8 2020 The addition of ATP restored the reduced IL-1beta secretion level from hemichannel inhibition. Adenosine Triphosphate 16-19 interleukin 1 alpha Homo sapiens 41-49 32538272-10 2020 Taken together, we conclude that hemichannels-mediated ATP release and subsequent NLRP3 inflammasome activation through P2X7R may be one mechanism by which MWCNTs induce macrophage IL-1beta secretion. Adenosine Triphosphate 55-58 interleukin 1 alpha Homo sapiens 181-189 32861242-10 2020 Upon exposure to pyroptotic stimuli (ATP or nigericin), human microglia displayed caspase-3/7 activation and cleavage of caspase-3/7-specific substrates (e.g., DFF45, ROCK1, and PARP), with accompanying features of pyroptosis including GSDMD immunopositive pyroptotic bodies, IL-1beta release, and membrane rupture. Adenosine Triphosphate 37-40 interleukin 1 alpha Homo sapiens 276-284 32312847-2 2020 IL-1beta expression and release are tightly controlled by changes in intracellular Ca2+ ([Ca2+]i), which has been associated with ATP release and purinergic signaling. Adenosine Triphosphate 130-133 interleukin 1 alpha Homo sapiens 0-8 32849554-2 2020 The NOD-, LRR- and pyrin domain containing protein 3 (NLRP3) is an innate immune signaling complex whose assembly and activation can be triggered by various signals ranging from microbial molecules to ATP or the abnormal accumulation of crystals, thus leading to IL-1beta and IL-18 maturation and secretion. Adenosine Triphosphate 201-204 interleukin 1 alpha Homo sapiens 263-271 32323100-8 2020 We found that co-treatment with LPS and ATP increased the secretion of IL-1beta and expression of NLRP3 in HPDLFs, while TRIM31 overexpression could reverse these effects caused by LPS and ATP. Adenosine Triphosphate 40-43 interleukin 1 alpha Homo sapiens 71-79 32076940-8 2020 Furthermore, SAL also decreased the activation of caspase-1 and inhibited the release of IL-1beta induced by lipopolysaccharide (LPS) and adenosine triphosphate (ATP) in human umbilical vein endothelial cell (HUVECs). Adenosine Triphosphate 138-160 interleukin 1 alpha Homo sapiens 89-97 32076940-8 2020 Furthermore, SAL also decreased the activation of caspase-1 and inhibited the release of IL-1beta induced by lipopolysaccharide (LPS) and adenosine triphosphate (ATP) in human umbilical vein endothelial cell (HUVECs). Adenosine Triphosphate 162-165 interleukin 1 alpha Homo sapiens 89-97 31580158-5 2019 Then, RT-PCR was performed to detect the effect of different concentrations of ATP on mRNA expression of IL-1beta and MCP-1 induced by LPS (1 mug/mL) and the TLR4 signaling pathway. Adenosine Triphosphate 79-82 interleukin 1 alpha Homo sapiens 105-113 31862710-1 2020 In response to extracellular ATP, the purinergic receptor P2X7 mediates various biological processes, including phosphatidylserine (PtdSer) exposure, phospholipid scrambling, dye uptake, ion transport, and IL-1beta production. Adenosine Triphosphate 29-32 interleukin 1 alpha Homo sapiens 206-214 31805552-3 2020 Here we show that in response to known inflammasome activators (ATP, nigericin) or the sialic acid-expressing human bacterial pathogen group B Streptococcus (GBS), the presence of Siglec-14 enhances, whereas Siglec-5 reduces, inflammasome activation and macrophage IL-1beta release. Adenosine Triphosphate 64-67 interleukin 1 alpha Homo sapiens 265-273 32230726-7 2020 However, application of exogenous control activators such as Nigericin or ATP to infected cells readily induced NLRP3 inflammasome formation and secretion of high amounts of mature IL-1beta. Adenosine Triphosphate 74-77 interleukin 1 alpha Homo sapiens 181-189 32554850-9 2020 As a result, IL-1beta increased NF-kappaB activation, IL-8 expression, intracellular and mitochondrial ROS levels, but decreased MMP and ATP level in A-T cells. Adenosine Triphosphate 137-140 interleukin 1 alpha Homo sapiens 13-21 31676289-13 2020 GENERAL SIGNIFICANCE: We propose that cell activation caused by MSU crystals induces peritoneal macrophages and THP-1 cells to release ATP and HMGB1, causing IL-1beta secretion via P2X7 receptor activation. Adenosine Triphosphate 135-138 interleukin 1 alpha Homo sapiens 158-166 31580158-9 2019 Only low concentration ATP (1, 10 muM) inhibited LPS-induced mRNA expression of IL-1beta and MCP-1. Adenosine Triphosphate 23-26 interleukin 1 alpha Homo sapiens 80-88 28539262-10 2017 In conclusion, we provide evidence that anti-endotoxin peptides inhibit the inflammasome/IL-1 axis induced by cytoplasmic LPS sensing in myeloid cells and keratinocytes and activation of the classical inflammasome by LPS/ATP which may contribute to the protection against bacterial sepsis and skin infections with intracellular Gram-negative bacteria. Adenosine Triphosphate 221-224 interleukin 1 alpha Homo sapiens 89-93 30803848-6 2019 SLE patients exhibit increased levels of ATP which binds to P2X receptors resulting in activation of the inflammasome and consequent release of IL-1beta and IL-18, cytokines associated with disease pathogenesis. Adenosine Triphosphate 41-44 interleukin 1 alpha Homo sapiens 144-152 31412063-7 2019 Treatment of HSVEC with exogenous ATP led to interleukin 1beta (IL-1beta) release and increased vascular cell adhesion molecule (VCAM) expression. Adenosine Triphosphate 34-37 interleukin 1 alpha Homo sapiens 64-72 29675024-5 2018 Then, we found that peripheral blood mononuclear cells (PBMCs) from IPF patients released IL-1alpha and IL-18 in a NLRP3- and calpain-independent manner after LPS +- ATP stimulation. Adenosine Triphosphate 166-169 interleukin 1 alpha Homo sapiens 90-99 25575516-8 2015 Moreover, ATP increased P2Y2-mediated upregulation of MUC8 expression; however, IL-1alpha significantly decreased the extent to which ATP/P2Y2 upregulated MUC8 expression. Adenosine Triphosphate 134-137 interleukin 1 alpha Homo sapiens 80-89 25730877-5 2015 In CAPS monocytes, LPS induces the externalization of copious amounts of ATP (10-fold), which drive IL-1beta, IL-18, and IL-1alpha release via activation of the P2X purinoceptor 7. Adenosine Triphosphate 73-76 interleukin 1 alpha Homo sapiens 121-130