Publikationsdatum:
2012-12-16
Beschreibung:
Vitamin D deficiency affects more that 1 billion people worldwide and is associated with an increased risk of developing a number of inflammatory/autoimmune diseases, including inflammatory bowel disease (IBD). At present, the basis for the impact of vitamin D on IBD and mucosal immune responses is unclear; however, IBD is known to reflect exaggerated immune responses to luminal bacteria, and vitamin D has been shown to play a role in regulating bacteria-host interactions. Therefore, to test the effect of active vitamin D on host responses to enteric bacteria, we gave 1,25(OH) 2 D 3 to mice infected with the bacterial pathogen Citrobacter rodentium , an extracellular microbe that causes acute colitis characterized by a strong Th1/Th17 immune response. 1,25(OH) 2 D 3 treatment of infected mice led to increased pathogen burdens and exaggerated tissue pathology. In association with their increased susceptibility, 1,25(OH) 2 D 3 -treated mice showed substantially reduced numbers of Th17 T cells within their infected colons, whereas only modest differences were noted in Th1 and Treg numbers. In accordance with the impaired Th17 responses, 1,25(OH) 2 D 3 -treated mice showed defects in their production of the antimicrobial peptide REG3. Taken together, these studies show that 1,25(OH) 2 D 3 suppresses Th17 T-cell responses in vivo and impairs mucosal host defense against an enteric bacterial pathogen.
Print ISSN:
0193-1857
Digitale ISSN:
1522-1547
Thema:
Medizin
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