Macrophage inflammatory protein-2 as mediator of inflammation in acute liver injury

查看全文 作　　者：Chao-Chao [1,2]Qin;Yan-Ning [1,2]Liu;Ying [1,2]Hu;Ying [1,2]Yang;Zhi [1,2]Chen

机构地区：[1]State Key Laboratory for Diagnosis and Treatment of Infectious Diseases,The First Affiliated Hospital,Zhejiang University School of Medicine;[2]Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases

出　　处：《World Journal of Gastroenterology》索引2017年第23卷第17期,共10页

基　　金：Supported by the State 12th 5-Year Plan S&T Projects of China,No.2012ZX10002007;National Natural Science Foundation of China,No.81272679,No.81470851 摘　　要：Macrophage inflammatory protein(MIP)-2 is one of the CXC chemokines and is also known as chemokine CXC ligand(CXCL2). MIP-2 affects neutrophil recruitment and activation through the p38 mitogen-activatedprotein-kinase-dependent signaling pathway, by binding to its specific receptors, CXCR1 and CXCR2. MIP-2 is produced by a variety of cell types, such as macrophages, monocytes, epithelial cells, and hepatocytes, in response to infection or injury. In liver injury, activated Kupffer cells are known as the major source of MIP-2. MIP-2-recruited and activated neutrophils can accelerate liver inflammation by releasing various inflammatory mediators. Here, we give a brief introduction to the basic molecular and cellular sources of MIP-2, and focus on its physiological and pathological functions in acute liver injury induced by concanavalin A, lipopolysaccharides, irradiation, ischemia/reperfusion, alcohol, and hypoxia, and hepatectomy-induced liver regeneration and tumor colorectal metastasis. Further understanding of the regulatory mechanisms of MIP-2 secretion and activation may be helpful to develop MIP-2-targeted therapeutic strategies to prevent liver inflammation. 关键词：巨噬细胞煽动性的 protein-2 肝损害 Polymorphonuclear neutrophils 巨噬细胞发炎

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Macrophage inflammatory protein-2 as mediator of inflammation in acute liver injury

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