{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,12]],"date-time":"2026-06-12T03:27:27Z","timestamp":1781234847088,"version":"3.54.1"},"reference-count":53,"publisher":"American Society for Microbiology","issue":"6","license":[{"start":{"date-parts":[[2015,6,1]],"date-time":"2015-06-01T00:00:00Z","timestamp":1433116800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Infect Immun"],"published-print":{"date-parts":[[2015,6]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            Activation of inflammasomes is an important aspect of innate immune responses to bacterial infection. Recent studies have linked\n            <jats:named-content content-type=\"genus-species\">Vibrio cholerae<\/jats:named-content>\n            secreted toxins to inflammasome activation by using murine macrophages. To increase relevance to human infection, studies of inflammasome-dependent cytokine secretion were conducted with the human THP-1 monocytic cell line and corroborated in primary human peripheral blood mononuclear cells (PBMCs). Both El Tor and classical strains of\n            <jats:named-content content-type=\"genus-species\">V. cholerae<\/jats:named-content>\n            activated ASC (apoptosis-associated speck-like protein-containing a CARD domain)-dependent release of interleukin-1\u03b2 (IL-1\u03b2) when cultured with human THP-1 cells, but the pattern of induction was distinct, depending on the repertoire of toxins the strains produced. El Tor biotype strains induced release of IL-1\u03b2 dependent on NOD-like receptor family pyrin domain-containing 3 (NLRP3) and ASC due to the secreted pore-forming toxin hemolysin. Unlike in studies with mouse macrophages, the MARTX toxin did not contribute to IL-1\u03b2 release from human monocytic cells. Classical biotype strains, which do not produce either hemolysin or the MARTX toxin, activated low-level IL-1\u03b2 release that was induced by cholera toxin (CT) and dependent on ASC but independent of NLRP3 and pyroptosis. El Tor strains likewise showed increased IL-1\u03b2 production dependent on CT when the hemolysin gene was deleted. In contrast to studies with murine macrophages, this phenotype was dependent on a catalytically active CT A subunit capable of inducing production of cyclic AMP and not on the B subunit. These studies demonstrate that the induction of the inflammasome in human THP-1 monocytes and in PBMCs by\n            <jats:named-content content-type=\"genus-species\">V. cholerae<\/jats:named-content>\n            varies with the biotype and is mediated by both NLRP3-dependent and -independent pathways.\n          <\/jats:p>","DOI":"10.1128\/iai.02461-14","type":"journal-article","created":{"date-parts":[[2015,4,7]],"date-time":"2015-04-07T01:42:15Z","timestamp":1428370935000},"page":"2496-2506","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":16,"title":["Mechanisms of Inflammasome Activation by Vibrio cholerae Secreted Toxins Vary with Strain Biotype"],"prefix":"10.1128","volume":"83","author":[{"given":"Jessica","family":"Queen","sequence":"first","affiliation":[{"name":"Department of Microbiology-Immunology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shivani","family":"Agarwal","sequence":"additional","affiliation":[{"name":"Department of Microbiology-Immunology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jazel S.","family":"Dolores","sequence":"additional","affiliation":[{"name":"Department of Microbiology-Immunology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christian","family":"Stehlik","sequence":"additional","affiliation":[{"name":"Department of Medicine, Division of Rheumatology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Karla J. 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