Abstract
Abstract Background: Ischemia-reperfusion injury (IRI) to the small intestine following clamping of the superior mesenteric artery (SMA) results in an intense local inflammatory response characterized by neutrophil infiltration and villous damage. IL-17A is a cytokine expressed by a variety of cells in response to inflammatory cytokines that are released following tissue injury and/or inflammation. IL-17A induces epithelial cells to secrete neutrophil chemoattractants, such as CXCL2. The cytokine IL-23, which can be produced by epithelial cells, plays an important role in IL-17A production. Objective: To test the hypothesis that IL-17A is critical for intestinal damage following IRI. Materials and Methods: IRI was induced in mice by SMA clamping. IL-17A deficient (Il17a-/-) and IL-23R deficient (Il23r-/-) mice. Intestinal injury was evaluated by Chiu scores of jejunal histological sections. Results: IRI was significantly less in both Il17a-/- mice and Il23r/- mice than in WT controls. We also found that pretreatment of WT mice with neutralizing antibody to IL-17A or IL-23 resulted in significant decrease in IRI compared to mice treated with isotype control antibody. Conclusions: These results indicate that IL-17A plays a critical role in IRI. They also suggest that IL-23 contributes to IRI, possibly by promoting IL-17A production.
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