Pulmonary collectin regulates drug-induced lung injury.

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The purposes of this project were to investigate the mechanisms of regulation by which lung collectins, surfactant proteins A and D (SP-A and SP-D), and Toll-like receptor (TLR) function against inflammation on the development of drug induced lung injury, and to establish the molecular basis for the clinical application of these proteins. First, the mouse model of lung injury was established using drugs, and SP-A^<-/-> mice had significantly higher mortality rates than WT mice. SP-A inhibited drug-induced inflammatory cytokine production from rat alveolar macrophages. SP-A blocked sTLR2-bleomycin binding in the dose dependent manner. These results suggest that bleomycin signals are transmitted through TLR2 dependent pathway and regulated by the molecular interaction of SP-A.