{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T18:21:33Z","timestamp":1791310893598,"version":"4.3.1"},"reference-count":45,"publisher":"National Academy of Sciences","issue":"50","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2004,12,14]]},"abstract":"<jats:p>\n                    Vi capsular polysaccharide (Vi) was first identified as a virulence antigen of\n                    <jats:italic>Salmonella typhi<\/jats:italic>\n                    , the causative agent of typhoid fever in humans; it renders\n                    <jats:italic>S. typhi<\/jats:italic>\n                    resistant to phagocytosis and the action of serum complement. However, the role of Vi during the infection of intestinal epithelium with\n                    <jats:italic>S. typhi<\/jats:italic>\n                    is not completely understood. We show here that Vi can interact with a model human intestinal epithelial cell line, Caco-2, through a cell-surface-associated molecular complex containing two major proteins of 30 and 35 kDa and a minor protein of \u224868 kDa. The two major proteins were identified as the putative tumor suppressor molecule, prohibitin, and its closely related homolog, B cell receptor-associated protein 37. These two proteins were enriched in lipid rafts, and Vi readily associated with these membrane microdomains. Engagement of Caco-2 cells with Vi inhibited their ability to produce an inflammatory response upon infection with Vi\n                    <jats:sup>\u2013<\/jats:sup>\n                    <jats:italic>S. typhi<\/jats:italic>\n                    . Consistent with this effect, infection of Caco-2 cells with Vi\n                    <jats:sup>+<\/jats:sup>\n                    <jats:italic>S. typhi<\/jats:italic>\n                    produced less IL-8 compared with Vi\n                    <jats:sup>\u2013<\/jats:sup>\n                    <jats:italic>S. typhi<\/jats:italic>\n                    . Cells treated with Vi showed reduced extracellular signal-regulated kinase phosphorylation in response to infection with Vi\n                    <jats:sup>\u2013<\/jats:sup>\n                    <jats:italic>S. typhi<\/jats:italic>\n                    or stimulation with phorbol 12-myristate 13-acetate, suggesting that the mitogen-activated protein kinase pathway might be a target for Vi-mediated inhibition of inflammatory responses. These findings reveal a crucial role for Vi in the modulation of early inflammatory responses during infection with\n                    <jats:italic>S. typhi<\/jats:italic>\n                    . This kind of a modulation could play a significant role in the establishment of infection by\n                    <jats:italic>S. typhi<\/jats:italic>\n                    .\n                  <\/jats:p>","DOI":"10.1073\/pnas.0407536101","type":"journal-article","created":{"date-parts":[[2004,12,2]],"date-time":"2004-12-02T20:30:15Z","timestamp":1102019415000},"page":"17492-17497","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":193,"title":["Vi polysaccharide of\n                    <i>Salmonella typhi<\/i>\n                    targets the prohibitin family of molecules in intestinal epithelial cells and suppresses early inflammatory responses"],"prefix":"10.1073","volume":"101","author":[{"given":"Amita","family":"Sharma","sequence":"first","affiliation":[{"name":"Hybridoma Laboratory, National Institute of Immunology, Aruna Asaf Ali Marg, New Delhi 110 067, India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ayub","family":"Qadri","sequence":"additional","affiliation":[{"name":"Hybridoma Laboratory, National Institute of Immunology, Aruna Asaf Ali Marg, New Delhi 110 067, India"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"341","published-online":{"date-parts":[[2004,12,2]]},"reference":[{"key":"e_1_3_2_1_2","doi-asserted-by":"publisher","DOI":"10.1038\/ni1102-1026"},{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.immunol.14.1.533"},{"key":"e_1_3_2_3_2","unstructured":"Keusch G. 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