Functional characterization of rat chemokine macrophage inflammatory protein-2

Frevert, Charles W.; Farone, Anthony L.; Danaee, Hadi; Paulauskis, Joseph; Kobzik, Lester

doi:10.1007/bf01534386

Cited by 81 publications

(58 citation statements)

References 10 publications

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“…1B). CXCR2 is a receptor for KC and MIP-2, which are potent neutrophil chemotactic factors (28,29,43) that we and others (12, 20, 38, 39, 49, 54, 55, 59, 60) observe to be induced by O 3 exposure. In both wild-type and CXCR2-deficient mice, Fig.…”

Section: Discussionmentioning

confidence: 70%

CXCR2 is essential for maximal neutrophil recruitment and methacholine responsiveness after ozone exposure

Johnston¹,

Mizgerd²,

Shore³

2005

American Journal of Physiology-Lung Cellular and Molecular Phys

104

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Section: Discussionmentioning

confidence: 70%

CXCR2 is essential for maximal neutrophil recruitment and methacholine responsiveness after ozone exposure

Johnston¹,

Mizgerd²,

Shore³

2005

American Journal of Physiology-Lung Cellular and Molecular Phys

104

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“…LIX expression in vivo has not been described previously. KC and MIP-2 have been evaluated in several mouse and rat models [23][24][25][26][27][28][29][30][31][32][33][34][35][36][37][38][39][40], but possible differences in the tissue distributions of KC and MIP-2 have not been systematically examined in the same model. Even if LIX, KC, and MIP-2 all prove to act exclusively via CXCR2, LIX might have biological functions distinct from KC and MIP-2 if it is predominantly expressed in different locations and regulated differently.…”

Section: Introductionmentioning

confidence: 99%

The murine neutrophil-chemoattractant chemokines LIX, KC, and MIP-2 have distinct induction kinetics, tissue distributions, and tissue-specific sensitivities to glucocorticoid regulation in endotoxemia

Rovai

Herschman

Smith

1998

Journal of Leukocyte Biology

171

144

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Lipopolysaccharide-induced CXC chemokine (LIX) is a novel murine neutrophil-chemoattractant CXC chemokine cloned as a glucocorticoidattenuated response gene. We investigated LIX message expression in an acute endotoxemia model. LIX message peaks later than KC or macrophage inflammatory protein-2 (MIP-2) and remains elevated longer in almost all tissues. Induced LIX message expression in heart is 5-to 6-fold greater than in lung and spleen, and 20-fold greater than in liver. In contrast, KC expression is equal in heart, lung, and liver, whereas MIP-2 expression is strongest in the lung. Glucocorticoid regulation of these genes also differs. Endotoxemia-induced LIX message expression in the lung is markedly enhanced in adrenalectomized mice and strongly attenuated by dexamethasone, whereas lung KC and MIP-2 expression are unaffected by glucocorticoids. It is surprising to note that endotoxemia-induced brain expression of LIX (but not KC or MIP-2) is increased by dexamethasone. These observations suggest that LIX may have biological roles distinct from KC and MIP-2. J. Leukoc. Biol. 64: 494-502; 1998.

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“…7,8 Furthermore, the expression of MIP-2 and KC are reported to increase during inflammation of the kidney, liver, and lung. [9][10][11][12] In the present study we investigate the roles of MIP-2 and KC in the local tissue injury induced by hepatic ischemia and reperfusion.…”

mentioning

confidence: 99%

Chemokine involvement in hepatic ischemia/reperfusion injury in mice: Roles for macrophage inflammatory protein-2 and kupffer cells

et al. 1998

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Hepatic injury induced by ischemia and reperfusion is an important clinical problem after liver resection or transplantation. Neutrophils are known to mediate the organ injury, but the precise mechanisms leading to hepatic neutrophil recruitment are undefined. Two CXC chemokines, macrophage inflammatory protein-2 (MIP-2) and KC, are potently chemotactic for neutrophils in vitro and have been reported to be involved in neutrophil-dependent inflammatory tissue injury. The objective of the present study was to determine the roles of MIP-2 and KC in the induction of hepatic ischemia/reperfusion injury. C57BL/6 mice were subjected to 90 minutes of partial hepatic ischemia followed by reperfusion. Hepatic injury was associated with neutrophil sequestration, edema, and elevated serum levels of hepatic transaminases. The expression of MIP-2 messenger RNA (mRNA) was induced within 3 hours after reperfusion, before any detectable increase in neutrophil accumulation, and was also increased to a greater extent in the ischemic lobe after 9 hours of reperfusion. These data suggest that MIP-2 may be involved in the initial recruitment of neutrophils to the ischemic lobe. In contrast, KC mRNA expression was not increased after 3 hours of reperfusion but after 9 hours increased equivalently in both ischemic and nonischemic lobes, suggesting a more generalized role in neutrophil recruitment. Neutralization of MIP-2 or KC resulted in significant decreases in hepatic neutrophil accumulation, edema, and hepatocellular injury. These data suggest that the local expression of MIP-2 and KC are important mediators involved in neutrophil-dependent hepatic injury induced by ischemia and reperfusion in mice. (HEPATOLOGY 1998;27:507-512.)Hepatic injury caused by ischemia and reperfusion during surgical resection or transplantation of the liver may lead to both local and systemic organ dysfunction. The local hepatic injury is comprised of two phases, with the initial injury being mediated by activated Kupffer cells. 1,2 Neutrophils are primed during this initial period and play a central role in the ensuing hepatic injury. The temporal involvement of Kupffer cells and neutrophils has been reported by studies in which neutropenic rats incurring hepatic ischemia and reperfusion experienced early injury but were protected from subsequent hepatic damage. 3 The accumulation of neutrophils may result in hepatic hypoperfusion, which is caused by sinusoidal occlusion, 4 and the release of reactive oxygen and proteases by neutrophils may also promote progressive hepatocellular damage. 5 However, the mechanisms by which ischemia and reperfusion induce neutrophil accumulation and the subsequent hepatic injury are undefined.Increased production of tumor necrosis factor-␣ is associated with neutrophil-dependent liver injury after hepatic ischemia and reperfusion. 6 The local production of tumor necrosis factor-␣ is increased after hepatic ischemia and reperfusion; and while tumor necrosis factor-␣ itself does not induce neutrophil chemotaxis, recent studi...

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Functional characterization of rat chemokine macrophage inflammatory protein-2

Cited by 81 publications

References 10 publications

CXCR2 is essential for maximal neutrophil recruitment and methacholine responsiveness after ozone exposure

CXCR2 is essential for maximal neutrophil recruitment and methacholine responsiveness after ozone exposure

The murine neutrophil-chemoattractant chemokines LIX, KC, and MIP-2 have distinct induction kinetics, tissue distributions, and tissue-specific sensitivities to glucocorticoid regulation in endotoxemia

Chemokine involvement in hepatic ischemia/reperfusion injury in mice: Roles for macrophage inflammatory protein-2 and kupffer cells

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