pi3k inhibition ameliorates acute lung injury through regulation of ibnfb pathway and innate immune responses background acute lung injury ali is a devastating disorder of the lung by various causes and its cardinal features are tissue inflammation pulmonary edema low lung compliance and widespread capillary leakage among phosphoinositide 3kinases pi3ks pi3k isoform has been shown to play an important role in a number of immuneinflammatory responsesmethods we investigated the role of pi3k and its molecular basis in lipopolysaccharide lpsinduced ali using a selective inhibitor for pi3k as 605240 and lpstreated c57bl6 miceresults treatment of mice with lps showed an increase of lung inflammation and vascular leakage production of reactive oxygen species ros interleukin il1 tumor necrosis factor and il4 adhesion molecule and vascular endothelial growth factor vegf was also increased administration of as 605240 to lpstreated mice markedly reduced the pathophysiological features of ali and the increased production of ros cytokines adhesion molecule and vegf in the lung our results also showed that treatment of mice with lps activates nuclear factorb nfb and degradation of inhibitory b ib through pi3k additionally infiltration of dendritic cells dcs and expression of tolllike receptor 4 tlr4 were significantly increased in the lung of lpstreated mice and inhibition of pi3k reduced the infiltration of dcs and tlr4 expression in the lungconclusions these results indicate that pi3k is critically involved in lpsinduced ali by regulating ibnfb pathway and innate immune responses based on our data we suggest that pi3k isoform is a promising target for the treatment of ali