MIP-2 ELISA Kit, Mouse

The acute release of neutrophils from the bone marrow is a critical step in their trafficking to sites of inflammation. This process is stimulated by systemically acting inflammatory mediators, such as the CXC chemokines. CXCL2/macrophage inflammatory protein (MIP)-2 is an inducible murine chemokine involved in attraction of polymorphonuclear granulocytes or T cells to sites of infection. Macrophages for example were shown to express large amounts of CXCL2/MIP-2 after stimulation with whole bacteria or bacterial cell wall components, e.g. lipopolysaccharide (LPS). CXCL2/MIP-2 induction was also observed in epithelial cells, vascular endothelial cells, astrocytes, mast cells and neutrophils. Additionally, proinflammatory cytokines like IL-1 and TNF-α were shown to induce CXCL2/MIP-2 expression in vitro in murine endothelial and epithelial cells. In vivo, in a model of ischemia/reperfusion, IL-1 was shown to be an important inducer of CXCL2/MIP-2 expression and subsequent hepatic neutrophil recruitment. It was demonstrated that MIP-2/CXCL2 expression is mediated by the p38 and SAPK/JNK pathway in mitogen-activated protein kinase signaling pathways, which activates NF-κB.²

CXCL2/MIP-2 and CXCL1/KC were shown to bind to the murine CXC receptor 2 (CXCR2), which is abundantly expressed on granulocytes and on NKT cells. When neutrophils from CXCR2 knock out mice were exposed to CXCL2/MIP-2 or CXCL1/KC no migration was observed, supporting the view that CXCR2 is the principal receptor for CXC chemokines on murine neutrophils. RhoA is part of a signaling pathway essential for aortic cell migration after CXCR2 ligation.³ In addition, CXCR2 activation might directly contribute to motor neuron degeneration. Thus, chemokines acting on CXCR2, including MIP-2, IL-8, may have direct pathogenic effects in CNS diseases, independent of the induction of leukocyte migration.⁴