Journal
WORLD JOURNAL OF GASTROENTEROLOGY
Volume 23, Issue 17, Pages 3043-3052Publisher
BAISHIDENG PUBLISHING GROUP INC
DOI: 10.3748/wjg.v23.i17.3043
Keywords
Macrophage inflammatory protein-2; Liver injury; Polymorphonuclear neutrophils; Macrophages; Inflammation
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Funding
- State 12th 5-Year Plan S&T Projects of China [2012ZX10002007]
- National Natural Science Foundation of China [81272679, 81470851]
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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.
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