Th e contribution of CD14 to TLR ligand-induced lung infl ammation has been investigated in several animal studies (Table 1) . Intratracheal administration of LPS did not signifi cantly induce TNF release and neutrophil accumulation in the lungs of rabbits, unless LPS was complexed with LBP [21] or the animals were subjected to mechanical ventilation [22] . Intratracheal instillation of anti-CD14 antibodies together with LPS/LBP or intravenous pretreatment with anti-CD14 or anti-TLR4 antibodies before mechanical ventilation markedly reduced these infl ammatory responses [21, 22] . Despite a reduction in lung neutrophil number, intravenous anti-CD14 treatment of rabbits exposed to LPS and subjected to ventilation did not cause a decrease in lung chemokines, including CXCL8 (IL-8), growth related oncogene (GRO) and monocyte chemoattractant protein (MCP)-1, whereas anti-TLR4 treatment did lower the level of GRO moderately and of CXCL8 signifi cantly [22] . Th ese fi ndings reveal that LPS alone does not cause signifi cant lung infl ammation in rabbits and suggest that additional accessory signals are required. Whether mechanical ventilation induces increased release of LBP or release of (endogenous) DAMPs which potentiate the LPS-induced response remains to be determined.