{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,12,19]],"date-time":"2025-12-19T21:07:36Z","timestamp":1766178456767,"version":"3.41.2"},"reference-count":56,"publisher":"American Society for Microbiology","issue":"1","license":[{"start":{"date-parts":[[2017,1,1]],"date-time":"2017-01-01T00:00:00Z","timestamp":1483228800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"funder":[{"name":"NSF"},{"DOI":"10.13039\/100000060","name":"HHS | NIH | National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","award":["AI080654"],"award-info":[{"award-number":["AI080654"]}],"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":[[2017,1]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            <jats:named-content content-type=\"genus-species\">Vibrio cholerae<\/jats:named-content>\n            is the causative bacteria of the diarrheal disease cholera, but it also persists in aquatic environments, where it displays an expression profile that is distinct from that during infection. Upon entry into the host, a tightly regulated circuit coordinates the induction of two major virulence factors: cholera toxin and a toxin-coregulated pilus (TCP). It has been shown that a set of bile salts, including taurocholate, serve as host signals to activate\n            <jats:named-content content-type=\"genus-species\">V. cholerae<\/jats:named-content>\n            virulence through inducing the activity of the transmembrane virulence regulator TcpP. In this study, we investigated the role of calcium, an abundant mental ion in the gut, in the regulation of virulence. We show that whereas Ca\n            <jats:sup>2+<\/jats:sup>\n            alone does not affect virulence, Ca\n            <jats:sup>2+<\/jats:sup>\n            enhances bile salt-dependent virulence activation for\n            <jats:named-content content-type=\"genus-species\">V. cholerae<\/jats:named-content>\n            . The induction of TCP by murine intestinal contents is counteracted when Ca\n            <jats:sup>2+<\/jats:sup>\n            is depleted by the high-affinity calcium chelator EGTA, suggesting that the calcium present in the gut is a relevant signal for\n            <jats:named-content content-type=\"genus-species\">V. cholerae<\/jats:named-content>\n            virulence induction\n            <jats:italic>in vivo<\/jats:italic>\n            . We further show that Ca\n            <jats:sup>2+<\/jats:sup>\n            enhances virulence by promoting bile salt-induced TcpP-TcpP interaction. Moreover, fluorescence recovery after photobleaching (FRAP) analysis demonstrated that exposure to bile salts and Ca\n            <jats:sup>2+<\/jats:sup>\n            together decreases the recovery rate for fluorescently labeled TcpP, but not for another inner membrane protein (TatA). Together, these data support a model in which physiological levels of Ca\n            <jats:sup>2+<\/jats:sup>\n            may result in altered bile salt-induced TcpP protein movement and activity, ultimately leading to an increased expression of virulence.\n          <\/jats:p>","DOI":"10.1128\/iai.00707-16","type":"journal-article","created":{"date-parts":[[2016,11,15]],"date-time":"2016-11-15T02:50:31Z","timestamp":1479178231000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":17,"title":["Calcium Enhances Bile Salt-Dependent Virulence Activation in Vibrio cholerae"],"prefix":"10.1128","volume":"85","author":[{"given":"Amanda J.","family":"Hay","sequence":"first","affiliation":[{"name":"Department of Microbiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, 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