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Interferons play opposing roles during inflammatory bowel disease

The contribution of the innate immune system to inflammatory bowel disease (IBD) is under intensive investigation. While research in animal models has demonstrated that type I interferons (IFN-Is) protect from IBD, studies of patients with IBD have produced conflicting results concerning the therapeutic potential of IFN-Is. Now a team of researchers based in Vienna with a contribution of the LBI-CR have resolved this issue.

They present data suggesting that IFN-Is play dual roles as regulators of intestinal inflammation in a mouse model of IBD, dextran sodium sulfate (DSS)-treated C57BL/6 mice. IFN-Is reduced acute intestinal damage and the abundance of colitis-associated intestinal bacteria caused by treatment with a high dose of DSS. However, they also inhibited the resolution of inflammation after DSS treatment. IFN-Is played an anti-inflammatory role by suppressing IL-1 signaling. Consistently, IL-1 receptor blockade reduced the severity of inflammation in IFN-I receptor-deficient mice and myeloid cell-restricted ablation of the IFN-I receptor was detrimental. The proinflammatory role of IFN-Is during recovery from DSS treatment was caused by IFN-I-dependent cell apoptosis as well as an increase in chemokine production and infiltrating inflammatory monocytes and neutrophils. Dagmar Stoiber of the LBI-CR and co-author on the report pointed out, that the reported findings may be important for guiding treatment strategies in patients, as IFN-Is play opposing roles in specific phases of intestinal injury and inflammation.

The report was published recently in the European Journal of Immunology.