title: Long-term selenium deficiency increases the pathogenicity of a Citrobacter rodentium infection in mice.
abstract: Citrobacter rodentium is a mouse pathogen that causes infectious colitis and shares characteristics with human enteropathogenic (EPEC) and enterohemorrhagic (EHEC) Escherichia coli, including the ability to cause attaching and effacing lesions in the colon and serves as a useful model to study the pathogenicity of these bacteria. In this study, mice were fed a selenium-deficient diet for 5 or 20 weeks and then infected with C. rodentium. Colonization of the colon by C. rodentium was similar in mice fed adequate or selenium-deficient diets, but total bacterial colonization of the spleen was elevated in mice fed selenium-deficient diet for 20 weeks. Infection-induced changes to the colon included inflammatory cell infiltration, gross changes in crypt architecture, and ulceration and denuding of the epithelial layer that were greatest in mice fed a selenium-deficient diet for 20 weeks. Expression of pro-inflammatory genes was significantly higher 12-days post-infection in mice fed the selenium-deficient diet for 20 weeks compared to mice fed a selenium-adequate diet or selenium-deficient diet for 5 weeks. Diarrhea was prevalent in mice fed the selenium-deficient diet for 20 weeks but not 5 weeks, and this was associated with decreased expression of solute carrier family 26a3 and carbonic anhydrase IV, genes involved in ion transport. These results indicated that selenium played an important role in resistance to the pathological effects of a C. rodentium infection, and therefore, selenium status may be important in the expression of human disease caused by common food-borne bacteria.
authors.affiliation: Agricultural Research Service, Beltsville Human Nutrition Research Center, Diet, Genomics, and Immunology Laboratory, United States Department of Agriculture, 10300 Baltimore Ave., B307C, Rm. 228, BARC-East, Beltsville, MD 20705, USA. allen.smith@ars.usda.gov
authors.forename: Allen D
authors.initials: AD
authors.lastname: Smith
authors.forename: Lumei
authors.initials: L
authors.lastname: Cheung
authors.forename: Sebastian
authors.initials: S
authors.lastname: Botero
mesh_terms: D000818:Animals; D000942:Antigens, Bacterial / Q000276:immunology; D018988:Bacterial Translocation; D001835:Body Weight / Q000502:physiology; D044082:Citrobacter rodentium / Q000472:pathogenicity*; D003106:Colon / Q000378:metabolism / Q000473:pathology; D018076:DNA, Complementary / Q000096:biosynthesis / Q000235:genetics; D004032:Diet; D060467:Disease Resistance / Q000502:physiology; D004756:Enterobacteriaceae Infections / Q000276:immunology / Q000382:microbiology* / Q000473:pathology; D041981:Gastrointestinal Tract / Q000276:immunology / Q000502:physiology; D015870:Gene Expression / Q000502:physiology; D005979:Glutathione Peroxidase / Q000378:metabolism; D008099:Liver / Q000201:enzymology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009929:Organ Size / Q000502:physiology; D012313:RNA / Q000096:biosynthesis / Q000235:genetics; D012643:Selenium / Q000172:deficiency*; D013154:Spleen / Q000502:physiology
chemical_list: D000942:Antigens, Bacterial; D018076:DNA, Complementary; D012313:RNA; D005979:Glutathione Peroxidase; D012643:Selenium