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

D. Huang, F. Fang, F. Xu

Department of Pediatric Intensive Care Unit, Guizhou Provincial People’s Hospital, GuiYang, China. xu_fengmail@163.com

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• Pharmacology

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 hyperoxia-induced inflammatory cytokines secretion.

RESULTS: Results of mRNA to protein level showed that elevated TLR2/4 activity and hyperoxia-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 hyperoxia stimulation, and the ROS inhibitor blocked TLR2/4 and NF-κB activity.

CONCLUSIONS: Data suggested that the TLR2/4-NF-κB pathway is involved in hyperoxia-induced inflammatory cytokines secretion in A549 human type II alveolar epithelial cells.

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