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INFLAMMATION/IMMUNITY/MEDIATORS

CD4⁺ T cells from IL-10-deficient mice transfer susceptibility to NSAID-induced Rag colitis

Department of Internal Medicine, University of Iowa, Iowa City, Iowa 52242

Submitted 18 December 2003 ; accepted in final form 23 January 2004

Products of arachidonic acid metabolism are important for mucosal homeostasis, because blockade of this pathway with an NSAID triggers rapid onset of severe colitis in the IL-10 knockout (IL-10^–/–) model of IBD. Rag mice do not make T or B cells. This study determined whether reconstitution of Rag mice with T cells from IL-10^–/– mice transferred NSAID colitis susceptibility. Rag mice were reconstituted by intraperitoneal injection with splenocytes from wild-type (WT) or IL-10^–/– animals. Colitis was induced by using piroxicam and was graded histologically. Isolated lamina propria mononuclear cells (LPMC), lamina propria T cells, and LPMC depleted of T cells from reconstituted Rag mice were studied for cytokine production. Only animals reconstituted with IL-10^–/– CD4⁺ T cells and administered piroxicam developed severe colitis. LPMC from these colitic animals made IFN-, whose production was dependent on T cells. Some IL-10 was produced but only from non-T cells. LPMC from the healthy Rag mice that were reconstituted with WT T cells and were piroxicam resistant made much more IL-10. This was mostly T cell dependent. In conclusion, only CD4⁺ T cells from IL-10^–/– animals leave Rag mice susceptible to NSAID-induced, Th1 colitis. Lamina propria T cells normally make large quantities of IL-10, suggesting that IL-10 from T cells may be protective.

interleukin-10; nonsteroidal anti-inflammatory drugs; inflammatory bowel disease

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