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Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2026,8,11]]},"abstract":"<jats:p>\n                    <jats:italic toggle=\"yes\">Salmonella enterica<\/jats:italic>\n                    serovar Typhimurium (\n                    <jats:italic toggle=\"yes\">S<\/jats:italic>\n                    Tm) infection triggers robust intestinal inflammatory responses during host colonization. Although host inflammatory responses typically function as defense mechanisms,\n                    <jats:italic toggle=\"yes\">S<\/jats:italic>\n                    Tm subverts these processes by co-opting inflammation-derived metabolites to increase both bacterial proliferation and intestinal colonization. Here, we demonstrate that\n                    <jats:italic toggle=\"yes\">S<\/jats:italic>\n                    Tm-induced intestinal inflammation results in the significant accumulation of luminal citrate, which plays dual roles in\n                    <jats:italic toggle=\"yes\">S<\/jats:italic>\n                    Tm pathogenesis, serving as both an anaerobic fermentation substrate to support bacterial growth and a virulence-activating signaling molecule. Mechanistically, the CitAB two-component system detects elevated citrate concentrations in the inflamed intestine, initiating the transcriptional activation of citrate fermentation genes to facilitate\n                    <jats:italic toggle=\"yes\">S<\/jats:italic>\n                    Tm luminal proliferation. Moreover, CitAB-mediated citrate sensing directly upregulates\n                    <jats:italic toggle=\"yes\">hilD<\/jats:italic>\n                    , which encodes the master regulator of\n                    <jats:italic toggle=\"yes\">Salmonella<\/jats:italic>\n                    Pathogenicity Island 1, thereby enhancing type III secretion system-dependent epithelial invasion. Genetic disruption of either citrate anaerobic fermentation pathway or citrate-mediated virulence-regulating pathway severely compromises both intestinal colonization and invasive capacity of\n                    <jats:italic toggle=\"yes\">S<\/jats:italic>\n                    Tm. These findings underscore citrate-responsive pathways as promising therapeutic targets for simultaneously disrupting\n                    <jats:italic toggle=\"yes\">S<\/jats:italic>\n                    Tm metabolic adaptability and virulence.\n                  <\/jats:p>","DOI":"10.1073\/pnas.2608715123","type":"journal-article","created":{"date-parts":[[2026,8,6]],"date-time":"2026-08-06T17:49:18Z","timestamp":1786038558000},"update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":0,"title":["Host inflammation\u2013derived citrate enhances\n                    <i>Salmonella<\/i>\n                    Typhimurium pathogenesis by fueling growth and activating virulence"],"prefix":"10.1073","volume":"123","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3141-0515","authenticated-orcid":false,"given":"Hongmin","family":"Sun","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/01y1kjr75","id-type":"ROR","asserted-by":"publisher"}],"name":"National Key Laboratory of Intelligent Tracking and Forecasting for Infectious Diseases, TEDA Institute of Biological Sciences and Biotechnology, Nankai University","place":["Tianjin, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0006-8348-0805","authenticated-orcid":false,"given":"Shuai","family":"Ma","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/01y1kjr75","id-type":"ROR","asserted-by":"publisher"}],"name":"National Key Laboratory of Intelligent Tracking and Forecasting for Infectious Diseases, TEDA Institute of Biological Sciences and Biotechnology, Nankai University","place":["Tianjin, 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