Product Sheet CL0452
Description
BACKGROUND Chemokines (chemotactic cytokines) are small heparin-binding proteins, which constitute a large family of peptides (60-100 amino acids) structurally related to cytokines whose main function is to regulate cell trafficking. They are subdivided into four families based on the number and spacing of the conserved cysteine residues in the N-terminus of the protein: CXC, CC, CX3C, and C, in agreement with the systematic nomenclature. Chemokines play a major role in selectively recruiting monocytes, neutrophils and lymphocytes as well as inducing chemotaxis through the activation of G-protein-coupled receptors (GPCR).1
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
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
REFERENCES
1. Gerard, C. & and Rollins, B.J.: Nature Immunol. 2:108-115, 2001
2. Kim, H.Y. & Kim, H.S.: Immunol. Cell Biol. 85:60-7, 2007
3. Moldobaeva, A. et al: Microvascul. Res. 75:53-8, 2008
4. De Paola, M. et al: Neuroimmunomodulation 14:310-16, 2008
2. Kim, H.Y. & Kim, H.S.: Immunol. Cell Biol. 85:60-7, 2007
3. Moldobaeva, A. et al: Microvascul. Res. 75:53-8, 2008
4. De Paola, M. et al: Neuroimmunomodulation 14:310-16, 2008
Products are for research use only. They are not intended for human, animal, or diagnostic applications.
(Click to Enlarge) Macrophage Inflammatory Protein 2 (MIP-2) ELISA Kit Standard Curve: Using the mouse MIP-2 ELISA Kit, O.D. data was graphed against MIP-2 protein concentration. The TMB reaction was incubated at 37°C for 15 min.
Details
Cat.No.: | CL0452 |
Target Protein Species: | Mouse |
Range: | 15.6pg/ml-1000pg/ml |
Specificity: | No detectable cross-reactivity with any other cytokine. |
Storage: | Store at 4°C. Use within 6 months. |
ELISA Kits are based on standard sandwich enzyme-linked immunosorbent assay technology. Freshly prepared standards, samples, and solutions are recommended for best results.
Products
| Product | Size | CAT.# | Price | Quantity |
|---|---|---|---|---|
| Mouse MIP-2 ELISA Kit: Mouse Macrophage Inflammatory Protein-2 ELISA Kit | Size: 96 Wells | CAT.#: CL0452 | Price: $490.00 |
Resources/Documents
Publications
2012
Lin, L., X. Zhao, W. Yan, and W. Qi. 2012. Influence of Orai1 intervention on mouse airway epithelium reactions in vivo and in vitro. Annals of Allergy, Asthma & Immunology, 108:103-112.e1.