To our knowledge, it is unclear whether CD14 contributes to host defense against Pseudomonas aeruginosa, a frequent cause of nosocomial pneumonia, and Burkholderia cepacia, a prevalent Gram-negative bacterium, together with P. aeruginosa, in patients with cystic fi brosis. Recently, it was found that both TLR4 and TLR5 are critical in the host response to P. aeruginosa and that TLR4-defi cient mice were not susceptible to intratracheal P. aeruginosa infection unless a bacterial mutant devoid of fl agellin production was used [36] . A similar approach is required to determine a role for CD14 in Pseudomonas-induced pneumonia. It is plausible that CD14 also contributes to the host response against B. cepacia, since LPS from this bacterium signals through TLR4 and anti-CD14 antibodies dramatically inhibited B. cepacia-induced chemokine secretion by lung epithelial cells [37] . Whether CD14 contributes to host defense response against Klebsiella pneumoniae, a known cause of nosocomial pneumonia, also remains to be determined, but data from our study with TLR4-mutant mice indicate that signaling through TLR4 is essential for successful clearance of this bacterium [38] .