{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,15]],"date-time":"2026-05-15T19:35:43Z","timestamp":1778873743417,"version":"3.51.4"},"reference-count":28,"publisher":"American Society for Microbiology","issue":"7","license":[{"start":{"date-parts":[[2015,7,1]],"date-time":"2015-07-01T00:00:00Z","timestamp":1435708800000},"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":[[2015,7]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:p>Vitamin A deficiency (A<jats:sup>\u2212<\/jats:sup>) remains a public health concern in developing countries and is associated with increased susceptibility to infection.<jats:named-content content-type=\"genus-species\">Citrobacter rodentium<\/jats:named-content>was used to model human<jats:named-content content-type=\"genus-species\">Escherichia coli<\/jats:named-content>infections. A<jats:sup>\u2212<\/jats:sup>mice developed a severe and lethal (40%) infection. Vitamin A-sufficient (A<jats:sup>+<\/jats:sup>) mice survived and cleared the infection by day 25. Retinoic acid treatment of A<jats:sup>\u2212<\/jats:sup>mice at the peak of the infection eliminated<jats:named-content content-type=\"genus-species\">C. rodentium<\/jats:named-content>within 16 days. Inflammation levels were not different between A<jats:sup>+<\/jats:sup>and A<jats:sup>\u2212<\/jats:sup>mouse colons, although the A<jats:sup>\u2212<\/jats:sup>mice were still infected at day 37. Increased mortality of A<jats:sup>\u2212<\/jats:sup>mice was not due to systemic cytokine production, an inability to clear systemic<jats:named-content content-type=\"genus-species\">C. rodentium<\/jats:named-content>, or increased pathogenicity. Instead, A<jats:sup>\u2212<\/jats:sup>mice developed a severe gut infection with most of the A<jats:sup>\u2212<\/jats:sup>mice surviving and resolving inflammation but not eliminating the infection. Improvements in vitamin A status might decrease susceptibility to enteric pathogens and prevent potential carriers from spreading infection to susceptible populations.<\/jats:p>","DOI":"10.1128\/iai.00201-15","type":"journal-article","created":{"date-parts":[[2015,5,12]],"date-time":"2015-05-12T02:12:30Z","timestamp":1431396750000},"page":"2984-2991","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":41,"title":["Vitamin A-Deficient Hosts Become Nonsymptomatic Reservoirs of Escherichia coli-Like Enteric Infections"],"prefix":"10.1128","volume":"83","author":[{"given":"Kaitlin L.","family":"McDaniel","sequence":"first","affiliation":[{"name":"Department of Veterinary and Biomedical Science, The Pennsylvania State University, University Park, Pennsylvania, USA"},{"name":"Pathobiology Graduate Program, The Pennsylvania State University, University Park, Pennsylvania, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Katherine H.","family":"Restori","sequence":"additional","affiliation":[{"name":"McGill University Health Centre, Montreal General Hospital, Montreal, Quebec, Canada"},{"name":"Research Institute of the McGill University Health Centre, Montreal General Hospital, Montreal, Quebec, Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jeffery W.","family":"Dodds","sequence":"additional","affiliation":[{"name":"Department of Veterinary and Biomedical Science, The Pennsylvania State University, University Park, Pennsylvania, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mary J.","family":"Kennett","sequence":"additional","affiliation":[{"name":"Department of Veterinary and Biomedical Science, The Pennsylvania State University, University Park, Pennsylvania, USA"},{"name":"Center for Molecular Immunology and Infectious Disease, The Pennsylvania State University, University Park, Pennsylvania, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"A. Catharine","family":"Ross","sequence":"additional","affiliation":[{"name":"Department of Nutritional Sciences, The Pennsylvania State University, University Park, Pennsylvania, USA"},{"name":"Center for Molecular Immunology and Infectious Disease, The Pennsylvania State University, University Park, Pennsylvania, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Margherita T.","family":"Cantorna","sequence":"additional","affiliation":[{"name":"Department of Veterinary and Biomedical Science, The Pennsylvania State University, University Park, Pennsylvania, USA"},{"name":"Center for Molecular Immunology and Infectious Disease, The Pennsylvania State University, University Park, Pennsylvania, USA"},{"name":"Pathobiology Graduate Program, The Pennsylvania State University, University Park, Pennsylvania, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"235","reference":[{"key":"e_1_3_3_2_2","volume-title":"Global prevalence of vitamin A deficiency in populations at risk 1995\u20132005: WHO global database on vitamin A deficiency","author":"WHO","year":"2009","unstructured":"WHO. 2009. 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