Our group determined whether CD14 also contributes to the development of lung infl ammation induced by LTA, a TLR2 ligand from the cell wall of Gram-positive bacteria [28, 29] . Lung infl ammation induced by Staphylo coccus aureus LTA was completely dependent on TLR2, but independent of LBP and only moderately dependent on CD14 expression. As compared to wildtype mice, S. aureus LTA-induced neutrophil infl ux was unchanged in CD14-defi cient mice, whereas TNF and CXCL2 release in the lung were partially reduced [28] . Strikingly, however, pulmonary infl ammation was also greatly diminished in TLR4-defi cient mice, as well as in mice defi cient for platelet activating factor receptor (PAFR), a known receptor for LTA on epithelial cells. Similarly, lung infl ammation induced by Streptococcus pneumoniae LTA, which is less potent compared S. aureus LTA, was also completely dependent on TLR2 expression. However, in contrast to S. aureus LTA, neutrophil infi ltration of the lung was moderately reduced in CD14-defi cent mice treated with pneumococcal LTA, whereas TNF and CXCL2 release in the lung was unchanged [29] . Moreover, pneumococcal LTAinduced lung infl ammation was moderately diminished in TLR4-defi cient mice. Th us, despite the amplifying eff ect on LTA-induced TLR2-mediated responses in vitro, CD14 contributes minimally to lung infl ammation induced by LTA. Th e unexpected contribution of TLR4 to LTA-induced lung infl ammation may result from DAMPs generated during the infl ammatory process in the respiratory tract.