Archives of medical research · 2009
Toll-like receptor 4 relates to lipopolysaccharide-induced mucus hypersecretion in rat airway.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Chen Lei, Wang Tao, Zhang Jian-Yong, Zhang Shang-Fu, Liu Dai-Shun, Xu Dan, Wang Xun, Chen Ya-Juan, Wen Fu-Qiang
Аннотация
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 1 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 <0.01) and AB/PAS-stained area (r = 0.781, p <0.01). 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.
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 1 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 <0.01) and AB/PAS-stained area (r = 0.781, p <0.01). 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.