TLRs 1-10 are expressed in lung tissue (45) , and individual TLRs are differentially regulated in specific lung cell populations in response to microbial stimula-tion. TLR2, TLR4, TLR5 and TLR9 are the most likely to be involved in recognition of bacteria in the lungs (46) (47) (48) . A study by Bernard et al. has shown that ALI/ ARDS induced by lipopolysaccharide (LPS) is a major cause of mortality among humans (49) . The LPS membrane receptor complex is composed of several accessory molecules, which include phosphatidylinositol-anchored CD14, TLR4, MD2 and MD1 (50) . The LPSbinding protein (LBP) enhances the binding of LPS to its receptor (51) . Absence of CD14, MD2 or LBP abrogates most LPS responses (51, 52) . Expression of functional TLR4 has been found in many cell types in the lung (45) , and LPS-induced lethal shock and ALI have been shown to be TLR4 dependent (53) (54) (55) . Thus, TLR4 plays a critical role in the mechanism of infection-related ALI.