{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T00:26:04Z","timestamp":1790727964161,"version":"4.1.0"},"reference-count":63,"publisher":"Oxford University Press (OUP)","issue":"3","license":[{"start":{"date-parts":[[2017,2,1]],"date-time":"2017-02-01T00:00:00Z","timestamp":1485907200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2017,2,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>NLRP3 inflammasome is a critical player in innate immunity. Neutrophil recruitment to tissues and effective neutrophil function are critical innate immune mechanisms for bacterial clearance. However, the role of NLRP3 in neutrophil-dependent bacterial clearance in polymicrobial sepsis is unclear. In this study, we evaluated the role of NLRP3 in polymicrobial sepsis induced by cecal ligation and puncture (CLP). Our results showed protection from death in NLRP3-deficient (Nlrp3\u2212\/\u2212) and NLRP3 inhibitor\u2013treated wild-type (C57BL\/6) mice. Nlrp3\u2212\/\u2212 and NLRP3 inhibitor\u2013treated mice displayed lower bacterial load but no impairment in neutrophil recruitment to peritoneum. However, neutrophil depletion abrogated protection from death in Nlrp3\u2212\/\u2212 mice in response to CLP. Intriguingly, following CLP, Nlrp3\u2212\/\u2212 peritoneal cells (primarily neutrophils) demonstrate decreased autophagy, augmented phagocytosis, and enhanced scavenger receptor (macrophage receptor with collagenous structure) and mannose-binding leptin expression. These findings enhance our understanding of the critical role of NLRP3 in modulating autophagy and phagocytosis in neutrophils and suggest that therapies should be targeted to modulate autophagy and phagocytosis in neutrophils to control bacterial burden in tissues during CLP-induced polymicrobial sepsis.<\/jats:p>","DOI":"10.4049\/jimmunol.1601745","type":"journal-article","created":{"date-parts":[[2016,12,29]],"date-time":"2016-12-29T02:00:16Z","timestamp":1482976816000},"page":"1253-1262","source":"Crossref","is-referenced-by-count":106,"title":["Deletion of <i>Nlrp3<\/i> Augments Survival during Polymicrobial Sepsis by Decreasing Autophagy and Enhancing Phagocytosis"],"prefix":"10.1093","volume":"198","author":[{"given":"Liliang","family":"Jin","sequence":"first","affiliation":[{"name":"Laboratory of Lung Biology, Department of Pathobiological Sciences and Center for Experimental Infectious Disease Research, School of Veterinary Medicine, Louisiana State University , Baton Rouge, LA 70803"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2182-5541","authenticated-orcid":false,"given":"Sanjay","family":"Batra","sequence":"additional","affiliation":[{"name":"Laboratory of Lung Biology, Department of Pathobiological Sciences and Center for Experimental Infectious Disease Research, School of Veterinary Medicine, Louisiana State University , Baton Rouge, LA 70803"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1959-1328","authenticated-orcid":false,"given":"Samithamby","family":"Jeyaseelan","sequence":"additional","affiliation":[{"name":"Laboratory of Lung Biology, Department of Pathobiological Sciences and Center for Experimental Infectious Disease Research, School of Veterinary Medicine, Louisiana State University , Baton Rouge, LA 70803"},{"name":"Division of Pulmonary and Critical Care, Department of Medicine, LSU Health Sciences Center , New Orleans, LA 70112"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2017,2,1]]},"reference":[{"key":"2025030615004852600_r1","doi-asserted-by":"crossref","first-page":"1303","DOI":"10.1097\/00003246-200107000-00002","article-title":"Epidemiology of severe sepsis in the United States: analysis of incidence, outcome, and associated costs of care","volume":"29","author":"Angus","year":"2001","journal-title":"Crit. 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