Toll-like Receptor 4 Relates to Lipopolysaccharide-induced Mucus Hypersecretion in Rat Airway

被引：33

作者：

Chen, Lei ^{[1
,2
]}

Wang, Tao ^{[1
,2
]}

Zhang, Jian-Yong ^{[1
,2
]}

Zhang, Shang-Fu ^{[3
]}

Liu, Dai-Shun ^{[1
,2
]}

Xu, Dan ^{[1
,2
]}

Wang, Xun ^{[1
,2
]}

Chen, Ya-Juan ^{[1
,2
]}

Wen, Fu-Qiang ^{[1
,2
]}

机构：

[1] Sichuan Univ, W China Sch Med, W China Hosp, Dept Resp Med, Chengdu 610041, Sichuan, Peoples R China

[2] Sichuan Univ, W China Sch Med, W China Hosp, State Key Lab Biotherapy China,Div Pulm, Chengdu 610041, Sichuan, Peoples R China

[3] Sichuan Univ, W China Sch Med, W China Hosp, Dept Pathol, Chengdu 610041, Sichuan, Peoples R China

来源：

ARCHIVES OF MEDICAL RESEARCH | 2009年 / 40卷 / 01期

基金：

中国国家自然科学基金;

关键词：

Airway mucus hypersecretion; Dexamethasone; Lipopolysaccharide; Toll-like receptor 4; MUC5AC MUCIN TRANSCRIPTION; GOBLET CELL METAPLASIA; SIGNAL-TRANSDUCTION; GENE-EXPRESSION; MESSENGER-RNA; DEXAMETHASONE; PROTEIN; KINASE; RECOGNITION; PATHWAY;

D O I：

10.1016/j.arcmed.2008.10.005

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：

Background. Toll-like receptor 4 (TLR4) is a transmembrane protein that participates in the recognition of lipopolysaccharide (LPS), a potentially important source of inflammation. To investigate the role of TLR4 in LPS-induced airway Mucus hypersecretion (AMH), we used a LPS-induced rat model treated with dexamethasone (DEX). Methods. Rats were randomly divided into four experimental groups: 1) saline (SA)treated with distilled water (DW) (control group); 2) LPS-treated with DW (LPS group); 3) LPS-treated with DEX (LPS plus DEX group); 4) SA-treated with DEX (DEX group). DEX (5 mg/kg) was intraperitoneally injected I h before being administered intratracheally with LPS. Expressions of TLR4 and MUC5AC were evaluated with RT-PCR, in situ hybridization, immunohistochemistry and Alcian blue/Periodic acid-schiff (AB/PAS) staining. Results. Increased expressions of TLR4 protein and mRNA were found in rat airway treated with LPS and peaked on day 2 after LPS administration. Following this, LPS increased MUC5AC expression and AB/PAS-stained goblet cells in rat airway. Correlation analysis showed TLR4 correlated well with the expression of MUC5AC (r = 0.684, p < 0.0 1) and AB/PAS-stained area(r = 0.781, p < 0.0 1). In addition, DEX pretreatment significantly reduced LPS-induced overexpression of TLR4 (p < 0.05) in rat airway. Conclusions. These results suggest TLR4 relates to LPS-induced AMH and support a role of TLR4 in DEX inhibition of LPS-induced AMH. (C) 2009 IMSS. Published by Elsevier Inc.

引用

页码：10 / 17

页数：8

共 27 条

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