Hyperoxia induces inflammation and regulates cytokine production in alveolar epithelium through TLR2/4-NF-kB-dependent mechanism

D Huang, F Fang, F Xu, Feng Xu
2016 unpublished
OBJECTIVE: It has been reported that inflammation of lung could be induced by proinflammatory factor under hyperoxia, which may be attributed by increasing generation of reactive oxygen species (ROS). MATERIALS AND METHODS: In the present study, with human epithelial lung cancer cell line A549 treated with hyperoxia as in vitro model , we found that hyperoxia stimulation induced TLR2/4 activity in A549 cells. ROS inhibitor NAC was used to investigate the role of ROS in hyper-oxia-induced
more » ... oxia-induced inflammatory cytokines secretion. RESULTS: Results of mRNA to protein level showed that elevated TLR2/4 activity and hy-peroxia-induced inflammatory cytokines secretion could be significantly attenuated by NAC. EMSA results showed the activation of nuclear factor-κB (NF-κB) increased after 2-h hyper-oxia stimulation, and the ROS inhibitor blocked TLR2/4 and NF-κB activity. CONCLUSIONS: Data suggested that the TL-R2/4-NF-κB pathway is involved in hyperoxia-induced inflammatory cytokines secretion in A549 human type II alveolar epithelial cells.
fatcat:plrcwsdlnvccjnwsmhk3vxq5ra