Abstract
G A A b st ra ct s Total RNA was extracted from cultured IMFs and HT-29 cells and the relative expression of mRNA for TL1A, DR3 and DcR3 (the decoy receptor for TL1A) was measured by realtime RT-PCR. Results: Stimulation of primary IMFs (or 18co cells) with IL-1a and/or TNFa resulted in significant upregulation of TL1A mRNA (P 3-fold increase over HC, P<0.05). Supernatants from cultures of TNF-α-stimulated HT-29 cells also induced the expression of TL1A in ISMFs (P<0.05 for any combination vs. unstimulated HT-29 cell supernatants). Finally, the expression of DR3 was significantly elevated in cultured HT-29 epithelial cells that were stimulated with the pro-inflammatory cytokines IL-1a, TNF-a, and IFN-g. Conclusions: Pro-inflammatory factors that are components of the mucosal milieu in CD induce the expression of TL1A in IMFs and of its functional receptor, DR3, in intestinal epithelial cells. Interactions between IMF-derived TL1A and its receptor, DR3 on epithelial cells may contribute to the pathogenesis of chronic intestinal inflammation.
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