摘要
Objective To confirm if pulmonary epithelial cells express Toll-like receptor 4 （TLR4） and investigate the role of TLR4 in airway inflammation of chronic obstructive pulmonary diseases （COPD）. Methods The expressions of TLR4, IL-8 mRNA and NF-KB activation stimulated by differen factors E lipopolysacharides （LPS）, interleukin-lβ, cigarette smoking extract （CSE）] in pulmonary epithelial cells were investigated. Results LPS, CSE and IL-lβ induced the production of IL-8 and activation of NF-KB. The levels of 1L-8 mRNA and NF-KB protein in E1A ＋ cell were markedly higher than E1A- cell and A549 cell （ P 〈0. 05）. The TLR4 mRNA of all the cells increased along with the increase of LPS＇ stimulated time. There was significant difference among different LPS＇ doses （ 12 h： P = O. 039 ; 24 h ： P = O. 013 ）. The TLR4 mRNA of E1A ＋ cell was higher than the other two groups （ P 〈0. 05）. IL-lβ induced all the cells expressing TLR4 mRNA. CSE had no effect on the expression of TLR4 mRNA. Conclusion Pulmonary epithelial cells express TLR4. LPS and IL-lβ up-regulate IL-8 mediated via the activation of NF-KB induced by TLR4. But CSE up-regulates IL-8 mediated via the activation of NF-KB, which has no relation to TLR4 and may have another signal transduction pathway.
Objective To confirm if pulmonary epithelial cells express Toll-like receptor 4 (TLR4) and investigate the role of TLR4 in airway inflammation of chronic obstructive pulmonary diseases (COPD). MethodsThe expressions of TLR4, IL-8 mRNA and NF-κB activation stimulated by differen factors [lipopolysacharides (LPS), interleukin-1β, cigarette smoking extract (CSE)] in pulmonary epithelial cells were investigated.Results LPS, CSE and IL-1β induced the production of IL-8 and activation of NF-κB. The levels of IL-8 mRNA and NF-κB protein in E1A+ cell were markedly higher than E1A- cell and A549 cell (P<0.05). The TLR4 mRNA of all the cells increased along with the increase of LPS’ stimulated time. There was significant difference among different LPS’ doses (12 h: P=0.039; 24 h: P=0.013). The TLR4 mRNA of E1A+ cell was higher than the other two groups (P<0.05). IL-1β induced all the cells expressing TLR4 mRNA. CSE had no effect on the expression of TLR4 mRNA. Conclusion Pulmonary epithelial cells express TLR4. LPS and IL-1β up-regulate IL-8 mediated via the activation of NF-κB induced by TLR4. But CSE up-regulates IL-8 mediated via the activation of NF-κB, which has no relation to TLR4 and may have another signal transduction pathway.
