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首页> 外文期刊>Journal of inflammation. >Annexin-A1 peptide down-regulates the leukocyte recruitment and up-regulates interleukin-10 release into lung after intestinal ischemia-reperfusion in mice
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Annexin-A1 peptide down-regulates the leukocyte recruitment and up-regulates interleukin-10 release into lung after intestinal ischemia-reperfusion in mice

机译：小鼠肠缺血-再灌注后Annexin-A1肽下调白细胞募集并上调白介素10释放入肺

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Background Intestinal ischemia/reperfusion (IR) injury is a serious and triggering event in the development of remote organ dysfunction, from which the lung is the main target. This condition is characterized by intense neutrophil recruitment, increased microvascular permeability. Intestinal IR is also responsible for induction of adult respiratory distress syndrome, the most serious and life-threatening form of acute lung injury. The purpose of this study was to investigate the effect of annexin-A1 protein as an endogenous regulator of the organ remote injury induced by intestinal ischemia/reperfusion. Male C57bl/6 mice were subjected to intestinal ischemia, induced by 45 min occlusion of the superior mesenteric artery, followed by reperfusion. Results The intestinal ischemia/reperfusion evoked a high intensity lung inflammation as indicated by the number of neutrophils as compared to control group. Treatment with annexin-A1 peptidomimetic Ac2-26, reduced the number of neutrophils in the lung tissue and increased its number in the blood vessels, which suggests a regulatory effect of the peptide Ac2-26 in the neutrophil migration. Moreover, the peptide Ac2-26 treatment was associated with higher levels of plasma IL-10. Conclusion Our data suggest that the annexin-A1 peptidomimetic Ac2-26 treatment has a regulatory and protective effect in the intestinal ischemia/reperfusion by attenuation of the leukocyte migration to the lung and induction of the anti-inflammatory cytokine IL-10 release into the plasma. The anti-inflammatory action of annexin-A1 and its peptidomimetic described here may serve as a basis for future therapeutic approach in mitigating inflammatory processes due to intestinal ischemia/reperfusion.
机译：背景肠道缺血/再灌注（IR）损伤是远端器官功能障碍发展中的一个严重触发事件，肺是主要目标。这种状况的特征是强烈的中性粒细胞募集，微血管通透性增加。肠道IR还负责诱发成人呼吸窘迫综合征，这是最严重且威胁生命的急性肺损伤形式。这项研究的目的是调查膜联蛋白A1蛋白作为肠缺血/再灌注所致器官远端损伤的内源性调节剂的作用。雄性C57bl / 6小鼠经历肠缺血，由肠系膜上动脉闭塞45分钟诱导，然后再灌注。结果与对照组相比，中性粒细胞数量表明肠缺血/再灌注引起高强度肺部炎症。用膜联蛋白-A1拟肽Ac2-26治疗减少了肺组织中嗜中性粒细胞的数量并增加了其在血管中的数量，这表明肽Ac2-26在嗜中性粒细胞迁移中具有调节作用。此外，肽Ac2-26处理与血浆IL-10水平升高有关。结论我们的数据表明，膜联蛋白A1拟肽Ac2-26治疗通过减少白细胞向肺的迁移并诱导抗炎性细胞因子IL-10释放到血浆中，对肠缺血/再灌注具有调节和保护作用。 。本文所述的膜联蛋白-A1及其拟肽的抗炎作用可作为减轻肠道缺血/再灌注引起的炎症过程的未来治疗方法的基础。

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