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Biochem. Biophys. Res. Commun. · Jun 2002
Role of CXC chemokines in the enhancement of LPS-induced neutrophil accumulation in the lung of mice by dexamethasone.
- Kimiko Aoki, Yumiko Ishida, Nana Kikuta, Hiroe Kawai, Mie Kuroiwa, and Hitoshi Sato.
- School of Pharmaceutical Sciences, Showa University, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo 142-8555, Japan. kaoki@pharm.showa-u.ac.jp
- Biochem. Biophys. Res. Commun. 2002 Jun 28; 294 (5): 1101-8.
AbstractLipopolysaccharide (LPS)-induced multiple organ injury was mediated in part by a transcription factor, nuclear factor-kappaB (NF-kappaB). Mice were pretreated with dexamethasone (DEX), an inhibitor of NF-kappaB activation, to elucidate its effects on LPS-induced early responses in vivo. Early responses measured 1 h after intraperitoneal LPS administration at a dose of 1 mg/kg were (1) neutrophil accumulation in the tissues, (2) neutrophil degranulation, and (3) protein and mRNA expressions of tumor necrosis factor-alpha (TNF-alpha) and ELR(+) CXC chemokines [macrophage inflammatory protein-2 (MIP-2) and cytokine-induced neutrophil chemoattractant (KC)]. Treatment with DEX before LPS administration suppressed NF-kappaB activation and plasma TNF-alpha levels almost to undetectable levels, but enhanced neutrophil accumulation and augmented MIP-2 levels in the lung. The suppression of plasma TNF-alpha levels by pretreatment with an anti-TNF-alpha antibody did not enhance LPS-induced neutrophil accumulation in the lung. These results demonstrate that the enhancement of LPS-induced neutrophil accumulation by DEX might be mediated by MIP-2 and not by TNF-alpha.
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