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Infect Immun. 2015 Jul;83(7):2984-91. doi: 10.1128/IAI.00201-15. Epub 2015 May 11.

Vitamin A-Deficient Hosts Become Nonsymptomatic Reservoirs of Escherichia coli-Like Enteric Infections.

Author information

1
Department of Veterinary and Biomedical Science, The Pennsylvania State University, University Park, Pennsylvania, USA Pathobiology Graduate Program, The Pennsylvania State University, University Park, Pennsylvania, USA.
2
McGill University Health Centre, Montreal General Hospital, Montreal, Quebec, Canada Research Institute of the McGill University Health Centre, Montreal General Hospital, Montreal, Quebec, Canada.
3
Department of Veterinary and Biomedical Science, The Pennsylvania State University, University Park, Pennsylvania, USA.
4
Department of Veterinary and Biomedical Science, The Pennsylvania State University, University Park, Pennsylvania, USA Center for Molecular Immunology and Infectious Disease, The Pennsylvania State University, University Park, Pennsylvania, USA.
5
Department of Nutritional Sciences, The Pennsylvania State University, University Park, Pennsylvania, USA Center for Molecular Immunology and Infectious Disease, The Pennsylvania State University, University Park, Pennsylvania, USA.
6
Department of Veterinary and Biomedical Science, The Pennsylvania State University, University Park, Pennsylvania, USA Center for Molecular Immunology and Infectious Disease, The Pennsylvania State University, University Park, Pennsylvania, USA Pathobiology Graduate Program, The Pennsylvania State University, University Park, Pennsylvania, USA mxc69@psu.edu.

Abstract

Vitamin A deficiency (A(-)) remains a public health concern in developing countries and is associated with increased susceptibility to infection. Citrobacter rodentium was used to model human Escherichia coli infections. A(-) mice developed a severe and lethal (40%) infection. Vitamin A-sufficient (A(+)) mice survived and cleared the infection by day 25. Retinoic acid treatment of A(-) mice at the peak of the infection eliminated C. rodentium within 16 days. Inflammation levels were not different between A(+) and A(-) mouse colons, although the A(-) mice were still infected at day 37. Increased mortality of A(-) mice was not due to systemic cytokine production, an inability to clear systemic C. rodentium, or increased pathogenicity. Instead, A(-) mice developed a severe gut infection with most of the A(-) 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.

PMID:
25964475
PMCID:
PMC4468526
DOI:
10.1128/IAI.00201-15
[Indexed for MEDLINE]
Free PMC Article

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