Macrophage inflammatory protein-2 as mediator of inflammation in acute liver injury.
Macrophage inflammatory protein-2 as mediator of inflammation in acute liver injury.
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DOI：
10.3748/wjg.v23.i17.3043
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发表时间：
2017-05-07
影响因子：
4.3
通讯作者：
Chen Z
中科院分区：
文献类型：
--
作者：
Qin CC;Liu YN;Hu Y;Yang Y;Chen Z
巨噬细胞炎症蛋白（MIP）-2是CXC趋化因子之一，也称为趋化因子CXC配体（CXCL 2）。MIP-2通过与其特异性受体CXCR 1和CXCR 2结合，通过p38丝裂原活化蛋白激酶依赖性信号通路影响中性粒细胞募集和活化。MIP-2由多种细胞类型产生，如巨噬细胞、单核细胞、上皮细胞和肝细胞，以响应感染或损伤。在肝损伤中，激活的枯否细胞被认为是MIP-2的主要来源。MIP-2募集和激活的中性粒细胞可以通过释放各种炎症介质加速肝脏炎症。本文就MIP-2的基本分子和细胞来源作一简要介绍，并着重阐述其在刀豆蛋白A、脂多糖、放射、缺血/再灌注、酒精、缺氧等诱导的急性肝损伤、肝切除诱导的肝再生和肿瘤结直肠转移中的生理和病理作用。进一步了解MIP-2的分泌和激活的调控机制可能有助于开发MIP-2靶向治疗策略以预防肝脏炎症。
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-activated-protein-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.