These include endotoxin-induced lipolysis leading to an increase in circulating fatty acids (48), which bind to the macrophage toll-like receptor 4 (TLR-4), thus limiting release of pro-inflammatory mediators, which reduces lung inflammation (49); impairment in the migration of neutrophils from bone marrow to target tissues (9); and the possibility that obese individuals have a metabolic reserve to counteract the increased catabolic stress of ARDS, because of additional energy stores in the form of adipose tissue (9). This evidence concerns the gene TLR4 and acute respiratory distress syndrome.