In addition to the evidence for TLR signaling in pulmonary epithelial cells in vitro, a variety of studies have shown that TLR activation may lead to the development of pulmonary inflammation in vivo. For instance, the TLR4 mutant strains C3H/HeJ and C57BL/10ScCr showed reduced clearance of pulmonary H. influenzae and E. coli (103, 104) . In an experimental Chlamydia pneumoniae pulmonary infection model, both TLR4 and TLR2 were found to be required for survival (105), while TLR4 and CD14 were found to play an important role in the response to respiratory syncytial virus (RSV) infection (106) . In response to pulmonary Streptococcus pneumoniae infection, TLR2-deficient mice revealed only modestly reduced inflammatory response and unchanged bacterial clearance (107) compared with wild-type counterparts. TLR3-deficient mice developed a survival advantage compared with wild-type mice, as well as reduced expression of IL-6 in the bronchoalveolar fluid in a murine model of influenza A virus infection (108) .