Glucocorticoids co-interact with lipoxin A4 via lipoxin A4 receptor (ALX) up-regulation

被引：29

作者：

Hashimoto, Atsushi

Murakami, Yousuke

Kitasato, Hidero

Hayashi, Izumi

Endo, Hirahito

机构：

[1] Kitasato Univ, Sch Med, Dept Rheumatol & Infect Dis, Sagamihara, Kanagawa 2288555, Japan

[2] RIKEN Res Ctr Allergy & Immunol, Res Unit Clin Immunol, Tsurumi Ku, Yokohama, Kanagawa 2300045, Japan

[3] Kitasato Univ, Sch Allied Hlth Sci, Dept Microbiol, Sagamihara, Kanagawa 2288555, Japan

[4] Nihon Pharmaceut Univ, Dept Pathophysiol, Saitama 3620806, Japan

来源：

BIOMEDICINE & PHARMACOTHERAPY | 2007年 / 61卷 / 01期

关键词：

glucocorticoid; lipoxin A(4); neutrophil;

D O I：

10.1016/j.biopha.2006.06.023

中图分类号：

R-3 [医学研究方法]; R3 [基础医学];

学科分类号：

1001 ;

摘要：

Lipoxin A(4) (LXA(4)) is an eicosanoid which is produced via lipoxygenases and characteristic of its anti-inflammatory effect in many metabolites of arachidonic acid, which are mostly pro-inflammatory. Glucocorticoids are well known also for their strong anti-inflammatory action but induce 5-lipoxygenase, essential to synthesize leukotrienes, which are pro-inflammatory. To elucidate the interaction of glucocorticoids and lipoxin A(4) for anti-inflammation, we analyzed in vitro expression of lipoxin A(4) receptor (ALX) on human neutrophils and the in vivo anti-inflammatory effect of glucocorticoids and LXA(4) using a dermal inflammation mouse model. ALX mRNA was up-regulated by dexamethasone (Dex) in human neutrophils. A glucocorticoid receptor antagonist, mifepristone, suppressed up-regulation of ALX induced by Dex. LXA(4) and/or Dex decreased CD11b expression on human neutrophils and suppressed mouse dermatitis induced by LTB4. These results suggest that anti-inflammatory effects of glucocorticoids depend at least partly on up-regulation of ALX and that the lipoxin system could be a negative feedback regulator for LTB4. (c) 2006 Elsevier Masson SAS. All rights reserved.

引用

页码：81 / 85

页数：5

共 22 条

[1] The antiglucocorticoid action of mifepristone [J].