{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,28]],"date-time":"2026-08-28T06:45:10Z","timestamp":1787899510233,"version":"build-2784847793"},"reference-count":47,"publisher":"American Society for Microbiology","issue":"9","license":[{"start":{"date-parts":[[2023,9,14]],"date-time":"2023-09-14T00:00:00Z","timestamp":1694649600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/doi.org\/10.1128\/ASMCopyrightv2"},{"start":{"date-parts":[[2023,9,14]],"date-time":"2023-09-14T00:00:00Z","timestamp":1694649600000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"funder":[{"name":"HHS | National Institutes of Health","award":["R01AI062859"],"award-info":[{"award-number":["R01AI062859"]}]},{"name":"HHS | National Institutes of Health","award":["R21AI083558"],"award-info":[{"award-number":["R21AI083558"]}]}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Infect Immun"],"published-print":{"date-parts":[[2023,9,14]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            <jats:italic>Salmonella enterica<\/jats:italic>\n            serovar Typhimurium is a leading cause of gastroenteritis worldwide and a deadly pathogen in children, immunocompromised patients, and the elderly.\n            <jats:italic>Salmonella<\/jats:italic>\n            induces innate immune responses through the NLRC4 inflammasome, which has been demonstrated to have distinct roles during systemic and mucosal detections of flagellin and non-flagellin molecules. We hypothesized that NLRC4 recognition of\n            <jats:italic>Salmonella<\/jats:italic>\n            flagellin is the dominant protective pathway during infection. To test this hypothesis, we used wild-type, flagellin-deficient, and flagellin-overproducing\n            <jats:italic>Salmonella<\/jats:italic>\n            to establish the role of flagellin in mediating NLRC4-dependent host resistance during systemic and mucosal infections in mice. We observed that during the systemic phase of infection,\n            <jats:italic>Salmonella<\/jats:italic>\n            efficiently evades NLRC4-mediated innate immunity. During mucosal\n            <jats:italic>Salmonella<\/jats:italic>\n            infection, flagellin recognition by the NLRC4 inflammasome pathway is the dominant mediator of protective innate immunity. Deletion of\n            <jats:italic>flgM<\/jats:italic>\n            results in constitutive expression of flagellin and severely limits systemic and mucosal\n            <jats:italic>Salmonella<\/jats:italic>\n            infections in an NLRC4 inflammasome-dependent manner. These data establish that recognition of\n            <jats:italic>Salmonella\u2019s<\/jats:italic>\n            flagellin by the NLRC4 inflammasome during mucosal infection is the dominant innate protective pathway for host resistance against the enteric pathogen and that FlgM-mediated evasion of the NLRC4 inflammasome enhances virulence and intestinal tissue destruction.\n          <\/jats:p>","DOI":"10.1128\/iai.00255-23","type":"journal-article","created":{"date-parts":[[2023,8,28]],"date-time":"2023-08-28T13:00:25Z","timestamp":1693227625000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":7,"title":["FlgM is required to evade NLRC4-mediated host protection against flagellated\n            <i>Salmonella<\/i>"],"prefix":"10.1128","volume":"91","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-6797-2179","authenticated-orcid":true,"given":"Am\u00e9rico 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