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Role of CXC chemokines in the enhancement of LPS-induced neutrophil accumulation in the lung of mice by dexamethasone.

Abstract：

:Lipopolysaccharide (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.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Aoki K,Ishida Y,Kikuta N,Kawai H,Kuroiwa M,Sato H

doi

10.1016/S0006-291X(02)00573-9

subject

Has Abstract

pub_date

2002-06-28 00:00:00

pages

1101-8

issue

5

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(02)00573-9

journal_volume

294

pub_type

杂志文章

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