{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,19]],"date-time":"2026-10-19T21:45:03Z","timestamp":1792446303487,"version":"4.5.0"},"reference-count":57,"publisher":"American Society for Microbiology","issue":"2","license":[{"start":{"date-parts":[[2015,2,1]],"date-time":"2015-02-01T00:00:00Z","timestamp":1422748800000},"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":[[2015,2]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Amyloids are proteins with cross-\u03b2-sheet structure that contribute to pathology and inflammation in complex human diseases, including Alzheimer's disease, Parkinson's disease, type II diabetes, and secondary amyloidosis. Bacteria also produce amyloids as a component of their extracellular matrix during biofilm formation. Recently, several human amyloids were shown to activate the NLRP3 inflammasome, leading to the activation of caspase 1 and production of interleukin 1\u03b2 (IL-1\u03b2). In this study, we investigated the activation of the NLRP3 inflammasome by bacterial amyloids using curli fibers, produced by\n                    <jats:named-content content-type=\"genus-species\">Salmonella enterica<\/jats:named-content>\n                    serovar Typhimurium and\n                    <jats:named-content content-type=\"genus-species\">Escherichia coli<\/jats:named-content>\n                    . Here, we show that curli fibers activate the NLRP3 inflammasome, leading to the production of IL-1\u03b2 via caspase 1 activation. Investigation of the underlying mechanism revealed that activation of Toll-like receptor 2 (TLR2) by curli fibers is critical in the generation of IL-1\u03b2. Interestingly, activation of the NLRP3 inflammasome by curli fibers or by amyloid \u03b2 of Alzheimer's disease does not cause cell death in macrophages. Overall, these data identify a cross talk between TLR2 and NLRP3 in response to the bacterial amyloid curli and generation of IL-1\u03b2 as a product of this interaction.\n                  <\/jats:p>","DOI":"10.1128\/iai.02370-14","type":"journal-article","created":{"date-parts":[[2014,11,24]],"date-time":"2014-11-24T23:04:41Z","timestamp":1416870281000},"page":"693-701","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":121,"title":["Toll-Like Receptor 2 and NLRP3 Cooperate To Recognize a Functional Bacterial Amyloid, Curli"],"prefix":"10.1128","volume":"83","author":[{"given":"Glenn J.","family":"Rapsinski","sequence":"first","affiliation":[{"name":"Department of Microbiology and Immunology, School of Medicine, Temple University, Philadelphia, Pennsylvania, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Meghan A.","family":"Wynosky-Dolfi","sequence":"additional","affiliation":[{"name":"Department of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gertrude O.","family":"Oppong","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, School of Medicine, Temple University, Philadelphia, Pennsylvania, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sarah A.","family":"Tursi","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, School of Medicine, Temple University, Philadelphia, Pennsylvania, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"R. 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