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• W2158191219 endingPage "499" @default.
• W2158191219 startingPage "492" @default.
• W2158191219 abstract "Abstract Ischemia reperfusion injury is characterized by local and systemic inflammation leading to considerable mortality. Previously, we have reported that soluble T1/ST2 (sST2), a member of the IL-1 receptor gene family, inhibits LPS-induced macrophage proinflammatory cytokine production. Here, we report the therapeutic effect of sST2-Fc in a murine model of intestinal ischemia reperfusion-induced injury. Administration of sST2-Fc fusion protein i.v., 10 min before reperfusion, reduced the production of TNF-α dose-dependently in the intestine and in the lungs. The sST2-Fc treatment with the highest dose (100 μg) resulted in inhibited vascular permeability, neutrophilia, and hemorrhage in the intestine and the lungs compared with controls treated with normal IgG. This was associated with down-regulated tissue levels of proinflammatory cytokines, markedly reduced serum TNF-α levels, and increased survival of mice from the sST2-Fc-treated group after ischemia and reperfusion injury. The beneficial effect of sST2-Fc treatment was associated with elevated IL-10 production in intestine and lung. sST2-Fc was not able to prevent the inflammatory response associated with intestinal ischemia and reperfusion in IL-10-deficient mice, suggesting that sST2 exerts its anti-inflammatory effect in a IL-10-dependent manner. These results also demonstrate that sST2-Fc may provide a novel, complementary approach in treating ischemic reperfusion injury." @default.
• W2158191219 created "2016-06-24" @default.
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• W2158191219 date "2006-11-10" @default.
• W2158191219 modified "2023-09-23" @default.
• W2158191219 title "ST2, an IL-1R family member, attenuates inflammation and lethality after intestinal ischemia and reperfusion" @default.
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• W2158191219 doi "https://doi.org/10.1189/jlb.0606422" @default.
• W2158191219 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/17099102" @default.
• W2158191219 hasPublicationYear "2006" @default.
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