{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T08:45:39Z","timestamp":1791276339845,"version":"4.1.0"},"reference-count":31,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2014,3,25]],"date-time":"2014-03-25T00:00:00Z","timestamp":1395705600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Clin Exp Pharma Physio"],"published-print":{"date-parts":[[2014,4]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p>\n<jats:list>\n\n<jats:list-item><jats:p>Adenosine triphosphate (<jats:styled-content style=\"fixed-case\">ATP<\/jats:styled-content>) has been described as a danger signal activating the <jats:styled-content style=\"fixed-case\">NOD<\/jats:styled-content>\u2010like receptor\u2010family protein\u00a03 (<jats:styled-content style=\"fixed-case\">NLRP<\/jats:styled-content>3)\u2010inflammasome leading to the pro\u2010inflammatory cytokine, interleukin (<jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>)\u20101\u03b2, release in the lung. The <jats:styled-content style=\"fixed-case\">NLRP<\/jats:styled-content>3\u2010inflammasome pathway has been previously described to be involved in experimental collagen deposition and the development of pulmonary fibrosis.<\/jats:p><\/jats:list-item>\n\n<jats:list-item><jats:p>The aim of the present study was to investigate the role of the <jats:styled-content style=\"fixed-case\">NLRP<\/jats:styled-content>3 inflammasome pathway and P2X7 purinergic receptor in the activation of human macrophages <jats:italic>in vitro<\/jats:italic> by <jats:styled-content style=\"fixed-case\">ATP<\/jats:styled-content>.<\/jats:p><\/jats:list-item>\n\n<jats:list-item><jats:p>We showed that adenosine 5\u2032\u2010[\u03b3\u2010thio]triphosphate tetralithium salt (<jats:styled-content style=\"fixed-case\">ATP<\/jats:styled-content>\u03b3S) and 2\u2032,3\u2032\u2010O\u2010(4\u2010benzoylbenzoyl) adenosine 5\u2032\u2010triphosphate (Bz<jats:styled-content style=\"fixed-case\">ATP<\/jats:styled-content>), two stable analogs of <jats:styled-content style=\"fixed-case\">ATP<\/jats:styled-content>, are able to potentiate the release of <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20101\u03b2 from human monocyte\u2010derived macrophages induced by low concentration of lipopolysaccharide (<jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content>). However, in the same conditions no increase in <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20101\u03b1 and <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20106 was observed. Immunochemistry has shown that human macrophages natively express <jats:styled-content style=\"fixed-case\">NLRP<\/jats:styled-content>3 and purinergic P2X<jats:sub>7<\/jats:sub> receptors (P2X<jats:sub>7<\/jats:sub>R). <jats:styled-content style=\"fixed-case\">NLRP<\/jats:styled-content>3 and <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20101\u03b2 m<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content> expression were induced from <jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content>\u2010primed macrophages, but also after 5\u2010h treatment of Bz<jats:styled-content style=\"fixed-case\">ATP<\/jats:styled-content> as analysed by reverse transcription quantitative polymerase chain reaction. However, other inflammasome pathways (<jats:styled-content style=\"fixed-case\">NLRP<\/jats:styled-content>1, <jats:styled-content style=\"fixed-case\">NLRP<\/jats:styled-content>2, <jats:styled-content style=\"fixed-case\">NLRC<\/jats:styled-content>4, <jats:styled-content style=\"fixed-case\">NLRP<\/jats:styled-content>6 and <jats:styled-content style=\"fixed-case\">AIM<\/jats:styled-content>2) and P2X<jats:sub>7<\/jats:sub>R were not induced by Bz<jats:styled-content style=\"fixed-case\">ATP<\/jats:styled-content>. We observed that P2X<jats:sub>7<\/jats:sub>R antagonists, A\u2010438079 and A\u2010740003, were able to reduce the release of <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20101\u03b2, but not of <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20101\u03b1 and <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20106 from macrophages stimulated by <jats:styled-content style=\"fixed-case\">ATP<\/jats:styled-content>\u03b3S or Bz<jats:styled-content style=\"fixed-case\">ATP<\/jats:styled-content>.<\/jats:p><\/jats:list-item>\n\n<jats:list-item><jats:p>The present results showed the involvement of the P2X<jats:sub>7<\/jats:sub>R\u2010<jats:styled-content style=\"fixed-case\">NLRP<\/jats:styled-content>3 inflammasome pathway in the secretion of <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20101\u03b2 from <jats:styled-content style=\"fixed-case\">ATP<\/jats:styled-content>\u2010stimulated human macrophages, and suggest that P2X<jats:sub>7<\/jats:sub>R were not involved in <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20101\u03b1 and <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20106 release. This study also points out that repression of the P2X<jats:sub>7<\/jats:sub>R represents a novel potential therapeutic approach to control fibrosis in lung injury.<\/jats:p><\/jats:list-item>\n<\/jats:list>\n<\/jats:p>","DOI":"10.1111\/1440-1681.12214","type":"journal-article","created":{"date-parts":[[2014,1,28]],"date-time":"2014-01-28T13:30:12Z","timestamp":1390915812000},"page":"279-286","source":"Crossref","is-referenced-by-count":42,"title":["Involvement of purinergic receptors and <scp>NOD<\/scp>\u2010like receptor\u2010family protein 3\u2010inflammasome pathway in the adenosine triphosphate\u2010induced cytokine release from macrophages"],"prefix":"10.1111","volume":"41","author":[{"given":"Thomas","family":"Gicquel","sequence":"first","affiliation":[{"name":"UMR991 INSERM\/University of Rennes 1 Rennes France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tatiana","family":"Victoni","sequence":"additional","affiliation":[{"name":"UMR991 INSERM\/University of Rennes 1 Rennes France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alain","family":"Fautrel","sequence":"additional","affiliation":[{"name":"UMR991 INSERM\/University of Rennes 1 Rennes France"},{"name":"Histopathological platform (H2P2) University of Rennes 1 Rennes France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sacha","family":"Robert","sequence":"additional","affiliation":[{"name":"UMR991 INSERM\/University of Rennes 1 Rennes France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Florence","family":"Gleonnec","sequence":"additional","affiliation":[{"name":"UMR991 INSERM\/University of Rennes 1 Rennes France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marie","family":"Guezingar","sequence":"additional","affiliation":[{"name":"UMR991 INSERM\/University of Rennes 1 Rennes France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Isabelle","family":"Couillin","sequence":"additional","affiliation":[{"name":"UMR7355INEM CNRS University of Orleans Orleans France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"V\u00e9ronique","family":"Catros","sequence":"additional","affiliation":[{"name":"UMR991 INSERM\/University of Rennes 1 Rennes France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elisabeth","family":"Boichot","sequence":"additional","affiliation":[{"name":"UMR991 INSERM\/University of Rennes 1 Rennes France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vincent","family":"Lagente","sequence":"additional","affiliation":[{"name":"UMR991 INSERM\/University of Rennes 1 Rennes France"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2014,3,25]]},"reference":[{"key":"e_1_2_7_2_1","doi-asserted-by":"publisher","DOI":"10.1038\/nature04516"},{"key":"e_1_2_7_3_1","doi-asserted-by":"publisher","DOI":"10.1038\/ng.285"},{"key":"e_1_2_7_4_1","doi-asserted-by":"publisher","DOI":"10.1136\/ard.2004.025577"},{"key":"e_1_2_7_5_1","doi-asserted-by":"publisher","DOI":"10.1016\/S1074-7613(04)00046-9"},{"key":"e_1_2_7_6_1","doi-asserted-by":"publisher","DOI":"10.1164\/rccm.200808-1274OC"},{"key":"e_1_2_7_7_1","doi-asserted-by":"publisher","DOI":"10.1164\/rccm.201003-0359OC"},{"key":"e_1_2_7_8_1","first-page":"3786","article-title":"IL\u20101R1\/MyD88 signaling and the inflammasome are essential in pulmonary inflammation and fibrosis in mice","volume":"117","author":"Gasse P","year":"2007","journal-title":"J. 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