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Heligmosomoides polygyrus inhibits established colitis in IL‐10‐deficient mice

Inflammatory bowel disease (IBD) is prevalent in industrialized countries, but rare in less‐developed countries. Helminths, common in less‐developed countries, may induce immunoregulatory circuits protective against IBD. IL‐10–/– mice given piroxicam develop severe and persistent colitis. Lamina propria mononuclear cells from colitic IL‐10–/– mice released IFN‐γ and IL‐12. The ongoing piroxicam‐induced colitis could be partially blocked with anti‐IL‐12 monoclonal antibody suggesting that the inflammation was at least partly IL‐12 dependent. Colonization of piroxicam‐treated colitic IL‐10–/– mice with Heligmosomoides polygyrus (an intestinal helminth) suppressed established inflammation and inhibited mucosal IL‐12 and IFN‐γ production. H. polygyrus augmented mucosal IL‐13, but not IL‐4 or IL‐5 production. Transfer of mesenteric lymph node (MLN) T cells from IL‐10–/– animals harboring H. polygyrus into colitic IL‐10–/– recipients inhibited colitis. MLN T cells from worm‐free mice did not. Foxp3 (scurfin) drives regulatory T cell function. H. polygyrus enhanced Foxp3 mRNA expression in MLN T cells that had regulatory activity. This suggests that H. polygyrus inhibits ongoing IL‐10–/– colitis in part through blocking mucosal Th1 cytokine production. Resolution of inflammation is associated with increased IL‐13 production and can be adoptively transferred by MLN T cells.