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本文综述了中性粒细胞在肝脏炎症中介导组织损伤的机制。中性粒细胞既参与宿主本身的防御反应,又因对某些致炎因素的过度反应而加重组织损伤。机体暴露于促炎症介质中会使中性粒细胞活化并聚集到肝脏脉管系统,实质细胞受损发出趋化信号激活中性粒细胞游走、脱颗粒释放蛋白酶和活性氧簇攻击靶细胞,引起细胞内氧化应激和线粒体机能障碍。此外有多种中性粒细胞源性的蛋白酶参与了中性粒细胞的游走和细胞毒性,同时通过对促炎症介质的加工而促进了炎症反应。另外,坏死细胞释放介质如高迁移率组信号-1也会进一步促进中性粒细胞介导的组织损伤。
This article reviews the mechanisms by which neutrophils mediate tissue damage in liver inflammation. Neutrophils not only participate in the host’s defensive response, but also aggravate tissue damage due to excessive reaction to certain inflammatory factors. Exposure of the body to proinflammatory mediators activates and accumulates neutrophils into the vasculature of the liver, where chemotaxis of the parenchymal cells triggers the migration of neutrophils, deglyasing the proteases and reactive oxygen species against target cells, Causing intracellular oxidative stress and mitochondrial dysfunction. In addition, a variety of neutrophil-derived proteases are involved in neutrophil migration and cytotoxicity, while promoting inflammatory responses through the processing of proinflammatory mediators. In addition, necrotic cell-releasing mediators, such as high-mobility group signal-1, further promote neutrophil-mediated tissue damage.