{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,30]],"date-time":"2025-10-30T17:05:29Z","timestamp":1761843929487},"reference-count":42,"publisher":"American Society for Microbiology","issue":"9","license":[{"start":{"date-parts":[[2009,9,1]],"date-time":"2009-09-01T00:00:00Z","timestamp":1251763200000},"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":[[2009,9]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            <jats:italic>Salmonella enterica<\/jats:italic>\n            , a gram-negative pathogen, causes a spectrum of human infections including enterocolitis and typhoid fever. We previously showed that\n            <jats:italic>Salmonella<\/jats:italic>\n            flagellin played a role in suppressing intestinal mucosal inflammation in a murine model of acute enterocolitis. In this study, we examined the role of flagellin in the typhoid-like systemic murine\n            <jats:italic>Salmonella<\/jats:italic>\n            infection by measuring bacterial proliferation, inflammation, leukocyte recruitment, and cellular apoptosis in Peyer's patches (PPs), mesenteric lymph node (MLN), and spleen. We found that relative to an isogenic wild-type (WT) strain, aflagellate\n            <jats:italic>Salmonella<\/jats:italic>\n            exhibited increased proliferation at 4 days postinfection in PPs and MLN but not spleen. The aflagellate mutant also elicited increased local and systemic secretion of inflammatory cytokines such as interleukin-1\u03b2, gamma interferon, and tumor necrosis factor alpha and enhanced surface expression of ICAM-1 on macrophages and dendritic cells (DCs). Furthermore, the recruitment of macrophages and DCs in PPs and MLN, but not spleen, was enhanced upon infection with aflagellate\n            <jats:italic>Salmonella<\/jats:italic>\n            . The relative differences between WT and aflagellate\n            <jats:italic>Salmonella<\/jats:italic>\n            were highly attenuated in Toll-like receptor 5-deficient (TLR5\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            ) mice, indicating involvement of TLR5-dependent signaling. Interestingly, infection with the aflagellate mutant also resulted in decreased levels of T-cell apoptosis in PPs relative to infection with WT\n            <jats:italic>Salmonella<\/jats:italic>\n            . We postulate that the initial lack of detection of the aflagellate mutant in the mucosa permits increased proliferation within the host and enhances inflammatory signaling in nonepithelial cell types, which subsequently promotes leukocyte recruitment. In contrast, lack of difference in any disease parameter measured in the spleen likely reflects that\n            <jats:italic>Salmonella<\/jats:italic>\n            expression of flagellin is downregulated in this organ. Thus, the characteristic inflammatory pathology of\n            <jats:italic>Salmonella<\/jats:italic>\n            infection occurs only in PPs and to a lesser extent in MLN during the initial phases of infection and these early responses are dependent on TLR5.\n          <\/jats:p>","DOI":"10.1128\/iai.00656-09","type":"journal-article","created":{"date-parts":[[2009,7,14]],"date-time":"2009-07-14T00:54:13Z","timestamp":1247532853000},"page":"4121-4129","update-policy":"http:\/\/dx.doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":25,"title":["Toll-Like Receptor 5-Dependent Regulation of Inflammation in Systemic\n            <i>Salmonella enterica<\/i>\n            Serovar Typhimurium Infection"],"prefix":"10.1128","volume":"77","author":[{"given":"Be\u0301ne\u0301dicte","family":"Fournier","sequence":"first","affiliation":[{"name":"Department of Pathology, Emory University School of Medicine, Atlanta, Georgia 30322"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ifor R.","family":"Williams","sequence":"additional","affiliation":[{"name":"Department of Pathology, Emory University School of Medicine, Atlanta, Georgia 30322"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Andrew T.","family":"Gewirtz","sequence":"additional","affiliation":[{"name":"Department of Pathology, Emory University School of Medicine, Atlanta, Georgia 30322"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Andrew S.","family":"Neish","sequence":"additional","affiliation":[{"name":"Department of Pathology, Emory University School of Medicine, Atlanta, Georgia 30322"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2958.1996.471410.x"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.174.12.7929"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2958.2006.05271.x"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2958.2004.04213.x"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2958.2003.03313.x"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.73.4.1907-1916.2005"},{"key":"e_1_3_2_8_2","doi-asserted-by":"publisher","DOI":"10.1038\/ni1346"},{"key":"e_1_3_2_9_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.167.4.1882"},{"key":"e_1_3_2_10_2","doi-asserted-by":"publisher","DOI":"10.1128\/jb.173.7.2301-2310.1991"},{"key":"e_1_3_2_11_2","doi-asserted-by":"publisher","DOI":"10.1007\/s000110050330"},{"key":"e_1_3_2_12_2","first-page":"131","volume":"289","year":"2005","unstructured":"Guiney, D. 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