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In addition to its direct toxicity, ethanol has two contrasting effects on the immune system: the nucleotide oligomerization domain\u2010like receptor pyrin domain\u2010containing\u20103 (\n                    <jats:styled-content style=\"fixed-case\">NLRP<\/jats:styled-content>\n                    3) inflammasome is inhibited by acute ethanol exposure but activated by chronic ethanol exposure. Purinergic receptors (especially the P2X7 receptor) are able to activate the\n                    <jats:styled-content style=\"fixed-case\">NLRP<\/jats:styled-content>\n                    3 inflammasome and are involved in many ethanol\u2010related diseases (such as gout, pulmonary fibrosis, alcoholic steatohepatitis, and certain cancers). We hypothesized that ethanol regulates purinergic receptors and thus modulates the\n                    <jats:styled-content style=\"fixed-case\">NLRP<\/jats:styled-content>\n                    3 inflammasome's activity. In experiments with monocyte\u2010derived macrophages, we found that interleukin (\n                    <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                    )\u20101\u03b2 secretion was inhibited after 7\u00a0h of exposure (but not 48\u00a0h of exposure) to ethanol. The disappearance of ethanol's inhibitory effect on\n                    <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                    \u20101\u03b2 secretion after 48\u00a0h was not mediated by the upregulated production of\n                    <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                    \u20101\u03b2,\n                    <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                    \u20101\u03b1,\n                    <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                    \u20106 or the inflammasome components\n                    <jats:styled-content style=\"fixed-case\">NLRP<\/jats:styled-content>\n                    3, apoptosis\u2010associated speck\u2010like protein containing a caspase recruitment domain, and caspase 1. P2X7R expression was upregulated by ethanol, whereas expression of the P2X4 and P2X1 receptors was not. Taken as a whole, our results suggest that ethanol induces\n                    <jats:styled-content style=\"fixed-case\">NLRP<\/jats:styled-content>\n                    3 inflammasome activation by upregulating the P2X7 receptor. This observation might have revealed a new mechanism for inflammation in ethanol\u2010related diseases.\n                  <\/jats:p>","DOI":"10.1111\/fcp.12433","type":"journal-article","created":{"date-parts":[[2018,11,17]],"date-time":"2018-11-17T15:34:05Z","timestamp":1542468845000},"page":"63-74","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":21,"title":["Ethanol upregulates the P2X7 purinergic receptor in human macrophages"],"prefix":"10.1111","volume":"33","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-5907-2450","authenticated-orcid":false,"given":"Brendan","family":"Le Dar\u00e9","sequence":"first","affiliation":[{"name":"INSERM INRA CHU Rennes Institut NuMeCan (Nutrition, Metabolism and Cancer) Univ Rennes F\u201035000 Rennes France"},{"name":"Pharmacy Service Pontchaillou University Hospital F\u201035000 Rennes 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