Cytokine-induced neutrophil chemoattractant

Blockade of a2, Pi and p2-adrenoreceptors on LPS-stimulated alveolar macrophages reduces the release of interleukin (IL)-ip, IL-6 and cytokine-induced neutrophil chemoattractant-1. In this same condition, TNFa release is also strongly reduced by a2 and p2-adrenoreceptors antagonists. However, the blockade of a2-adrenoreceptors reached the most consistent suppression of the investigated cytokines (Flierl et al., 2007). 

Zagorski, J. and Wahl, S. M. (1997) Inhibition of acute peritoneal inflammation in rats by a cytokine induced neutrophil chemoattractant receptor antagonist. J. Immunol. 159, 1059-1062. 

T. Liu, P. R. Young, P. C. McDonnell, R. F. White, F. C. Barone, and G. Z. Feuerstein, Cytokine-Induced Neutrophil Chemoattractant mRNA Expressed in Cerebral Ischemia, Neuroscience Letters, 164(1993) 125-128. 

Y. Yamasaki, Y. Matsuo, N. Matsuura, H. Onodera, Y. Itoyama, and K. Kogure, Transient Increase of Cytokine-Induced Neutrophil Chemoattractant, A Member of the Interleukin-8 Family, in Ischemic Brain Areas After Focal Ischemia in Rats, Stroke, 26 (1995) 318-323. 

Cytokine Production/Cellular Activation TNFa and IFNy mediate the induction of other cytokines (IL-1 and IL-6) and the activation of phagocytes. It has been suggested that particle-induced expression of MIP-2 and cytokine-induced neutrophil chemoattractant CKs in the rat lung are mediated at least in part by production of TNFa. TNF is involved in control of monocyte-mediated regulation of cytokine production by T cells. Preincubation of monocytes with rTNF enhanced their ability to induce IFNy production, and TNF synthesis inhibitors decreased this induction. However, Th2 cells are stimulated in the relative absence of monocyte co-stimulatory signal(s), probably IL-6. Concerning pain responsivity, TNFa produces dose-dependent hyperalgesia mediated via the induced release of IL-lp. ... 

Yamasaki, Y., Matsuo, Y., Matsuura, N., Onodera, H., Itoyama, Y., and Kogure, K., Transient increase of cytokine-induced neutrophil chemoattractant, a member of the interleukin-8 family, in ischaemic brain areas after focal ischaemia in rats, Stroke, 26, 318, 1995. 

Koto H, Salmon M, Haddad el-B, Huang TJ, Zagorski J, Chung KF. Role of cytokine-induced neutrophil chemoattractant (CINC) in ozone-induced airway inflammation and hyperresponsiveness. Am J Respir Crit Care Med 1997 156 234—239. 

Cytokine-induced neutrophil chemoattractant production in lipopolysaccharide-stimulated rat alveolar macrophages is regulated by the polyamine, putrescine (Kamoi et al. 1997). 

Crippen TL, Klasing KC, Hyde DM. Cytokine-induced neutrophil chemoattractant production by primary rat alveolar type It eells. Inflammation 1995 19 575-586. 

Watanabe K, Kinoshita S, Nakagaw H. Purification and characterization of cytokine-induced neutrophil chemoattractant produced by epithelioid cell line of normal rat kidney. Biochem Biophys Res Commim 1989 161 1093 1099. 

The failure of antioxidant mechanisms to correct redox disequilibrium could lead to the escalation of oxidative to tier 2. Tier 2 cellular responses are characterized by the activation of cellular signaling pathway such as stress-activated kinases (p38 MAP kinase and JNK) along with activation and nuclear translocation of transcription factors NF-kB and STAT-1. NF-KB-induced transcriptional activation leads to the production of a number of pro-inflammatory cytokines, including the neutrophil chemoattractant IL-8. STAT-1 activation stimulates the increased production of CXC-motif chemokines that function in lymphocyte recruitment and activation. Therefore, tier 2 oxidative responses result in an inflammatory response in the lung. 

Over the past ten years, more than 40 unique human and murine cytokines have been identified as members of chemokine superfamily of chemoattractants. These cytokines have been shown to induce the directional migration of selected cell types including neutrophils, monocytes, macrophages, dendritic cells, lymphocytes, basophils, eosinophils, and fibroblasts. 

IL-17 induces the production of IL-8 in endothelial and parenchymal cells, indicating an indirect role in PMN recruitment. IL-8 is a potent chemoattractant for polymorphonuclear neutrophils (PMN) and can also stimulate the release of neutrophil granules and the respiratory burst of these cells [5,71-78]. In their study, Kostulas et al. found that the proinflammatory cytokine IL-17 was elevated systemically after ischemic stroke. IL-17 induces the secretion of cytokines, including IL-8, and enhances the expression of ICAM-1 in cultures of stromal cells and human fibroblasts [5,77,79]. 

Ogata H, Takeya M, Yrshimura T, Takagi K, Takahashi K The role of monocyte chemoattractant protein-1 (MCP-1) in the pathogenesis of collagen-induced arthritis in rats. J Pathol 1997 182 106-114. Yamashiro S, Kamohara H, Yoshimura T MCP-1 is selectively expressed in the late phase by cytokine-stimulated human neutrophils TNF-alpha plays a role in maximal MCP-1 mRNA expression. J Leukoc Biol 1999 65 671-679. 

Neutrophil depletion prevents development of cerebral malaria caused by P berghei ANKA and decreases sequestration of monocytes and microhemorrhage in the brain [87]. This is associated with downregulated levels of IFN-7, TNF-a, IL-2, and IL-12 p40 in the brain, with no corresponding Th2 cytokine increases. Peritoneal exudate neutrophils, obtained after intraperitoneal injection of P berghei ANKA-parasitized red blood cells, contain IL-12 p40 mRNA, but it is not clear whether this represents parasite-induced or preformed IL-12 message [88]. Likewise, the PMN were found also to express mRNA for IL-18, IL-10, IFN-7 and TNF-a, and the Thl chemoattractants MIG, MIP-la, and IP-10. 

Cathepsin G is a potent chemoattractant for monocytes, macrophages and T cells, and has been implicated as a neutrophil-derived signal that induces mononuclear cell and T-cell-dependent immune responses [17], Both cathepsin G and a defensins stimulate IFN-y and IL-4 cytokine production by immune spleen cells by enhancing either the Thl or the Th2 limb of the immune response [17],... 

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