Abstract
Abstract Ischemia reperfusion injury is a type of injury seen in clinical conditions, such as trauma, hemorrhagic shock, organ transplantation, revascularization processes, and autoimmune diseases like systemic lupus erythematosus. MRL/lpr mice due to their autoimmune background present with accelerated mesenteric ischemia reperfusion injury (IR/I). To evaluate the effect of complement inhibition on tissue damage after mesenteric IR in MRL/lpr mice, we depleted complement using Cobra Venom factor (CVF) or blocked C5a receptor with a C5aR antagonist, and performed intestinal ischemia reperfusion. First, we confirmed that CVF treatment completely depleted C3 from the mice serum. Next, we found that the treatment with either CVF or C5aR antagonist attenuated intestinal injury following intestinal IR. Notably, depletion of complement increased the presence of IL-10 producing CD4+ cells (Tr1) and IL-10 producing Th17 cells in the intestine. These results suggest that complement may regulate the T-cell response during intestinal ischemia reperfusion injury.
Published Version
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