Mechanical ventilation (MV) provides life-saving support for many patients with respiratory failure (137) . However, mechanical stresses produced by MV can induce lung injury, termed ventilator-induced lung injury (138) . Evidence from animal experimental studies has demonstrated that MV per se can induce inflammatory responses (139) (140) (141) . A recent report has demonstrated that TLR4, but not TLR2, played a role in development of the inflammatory response after shorttime MV (142) . MV not only causes ventilator-induced lung injury in healthy animals, but also exacerbates damage in the injured lung (143) . TLR4 blockade reduces pulmonary inflammation caused by the combination of LPS and MV (144) . In the mechanism of hyperoxia-induced ALI, TLR3 expression and activation seems impotent. Exposure of human epithelial cells to hyperoxia in the absence of an exogenous viral pathogen significantly increased TLR3 expression. In vivo studies showed that both the absence of TLR3 via gene deletion in mice and the presence of an anti-TLR3 antibody in wild-type mice conferred significant protection in a hyperoxia-mediated lung injury model (145) .