{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,27]],"date-time":"2026-09-27T10:52:26Z","timestamp":1790506346522,"version":"4.1.0"},"reference-count":40,"publisher":"American Society for Microbiology","issue":"11","license":[{"start":{"date-parts":[[2016,11,1]],"date-time":"2016-11-01T00:00:00Z","timestamp":1477958400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"funder":[{"DOI":"10.13039\/100000060","name":"HHS | NIH | National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","award":["AI109002"],"award-info":[{"award-number":["AI109002"]}],"id":[{"id":"10.13039\/100000060","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000060","name":"HHS | NIH | National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","award":["AI116917"],"award-info":[{"award-number":["AI116917"]}],"id":[{"id":"10.13039\/100000060","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Infect Immun"],"published-print":{"date-parts":[[2016,11]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            <jats:named-content content-type=\"genus-species\">Salmonella enterica<\/jats:named-content>\n            serovar Typhi, the causative agent of typhoid fever in humans, forms biofilms encapsulated by an extracellular matrix (ECM). Biofilms facilitate colonization and persistent infection in gallbladders of humans and mouse models of chronic carriage. Individual roles of matrix components have not been completely elucidated\n            <jats:italic>in vitro<\/jats:italic>\n            or\n            <jats:italic>in vivo<\/jats:italic>\n            . To examine individual functions, strains of\n            <jats:named-content content-type=\"genus-species\">Salmonella enterica<\/jats:named-content>\n            serovar Typhimurium, the murine model of\n            <jats:italic>S<\/jats:italic>\n            . Typhi, in which various ECM genes were deleted or added, were created to examine biofilm formation, colonization, and persistence in the gallbladder. Studies show that curli contributes most significantly to biofilm formation. Expression of Vi antigen decreased biofilm formation\n            <jats:italic>in vitro<\/jats:italic>\n            and virulence and bacterial survival\n            <jats:italic>in vivo<\/jats:italic>\n            without altering the examined gallbladder pro- or anti-inflammatory cytokines. Oppositely, loss of all ECM components (\u0394\n            <jats:italic>wcaM<\/jats:italic>\n            \u0394\n            <jats:italic>csgA<\/jats:italic>\n            \u0394\n            <jats:italic>yihO<\/jats:italic>\n            \u0394\n            <jats:italic>bcsE<\/jats:italic>\n            ) increased virulence and bacterial survival\n            <jats:italic>in vivo<\/jats:italic>\n            and reduced gallbladder interleukin-10 (IL-10) levels. Colanic acid and curli mutants had the largest defects in biofilm-forming ability and contributed most significantly to the virulence increase of the \u0394\n            <jats:italic>wcaM<\/jats:italic>\n            \u0394\n            <jats:italic>csgA<\/jats:italic>\n            \u0394\n            <jats:italic>yihO<\/jats:italic>\n            \u0394\n            <jats:italic>bcsE<\/jats:italic>\n            mutant strain. While the \u0394\n            <jats:italic>wcaM<\/jats:italic>\n            \u0394\n            <jats:italic>csgA<\/jats:italic>\n            \u0394\n            <jats:italic>yihO<\/jats:italic>\n            \u0394\n            <jats:italic>bcsE<\/jats:italic>\n            mutant was not altered in resistance to complement or growth in macrophages, it attached and invaded macrophages better than the wild-type (WT) strain. These data suggest that ECM components have various levels of importance in biofilm formation and gallbladder colonization and that the ECM diminishes disseminated disease in our model, perhaps by reducing cell attachment\/invasion and dampening inflammation by maintaining\/inducing IL-10 production. Understanding how ECM components aid acute disease and persistence could lead to improvements in therapeutic treatment of typhoid fever patients.\n          <\/jats:p>","DOI":"10.1128\/iai.00532-16","type":"journal-article","created":{"date-parts":[[2016,9,7]],"date-time":"2016-09-07T01:30:00Z","timestamp":1473211800000},"page":"3243-3251","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":56,"title":["Salmonella Extracellular Matrix Components Influence Biofilm Formation and Gallbladder Colonization"],"prefix":"10.1128","volume":"84","author":[{"given":"Haley E.","family":"Adcox","sequence":"first","affiliation":[{"name":"Center for Microbial Interface Biology, Department of Microbial Infection and Immunity, The Ohio State University, Columbus, Ohio, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Erin M.","family":"Vasicek","sequence":"additional","affiliation":[{"name":"Center for Microbial Interface Biology, Department of Microbial Infection and Immunity, The Ohio State University, Columbus, Ohio, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Varun","family":"Dwivedi","sequence":"additional","affiliation":[{"name":"Center for Microbial Interface Biology, Department of Microbial Infection and Immunity, The Ohio State University, Columbus, Ohio, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ky V.","family":"Hoang","sequence":"additional","affiliation":[{"name":"Center for Microbial Interface Biology, Department of Microbial Infection and Immunity, The Ohio State University, Columbus, Ohio, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joanne","family":"Turner","sequence":"additional","affiliation":[{"name":"Center for Microbial Interface Biology, Department of Microbial Infection and Immunity, The Ohio State University, Columbus, Ohio, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"John S.","family":"Gunn","sequence":"additional","affiliation":[{"name":"Center for Microbial Interface Biology, Department of Microbial Infection and Immunity, The Ohio State University, Columbus, Ohio, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_3_2_2","first-page":"346","article-title":"The global burden of typhoid fever","volume":"82","author":"Crump JA","year":"2004","unstructured":"Crump JA, Luby SP, Mintz ED. 2004. 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