Lipopolysaccharide-induced acute lung injury is lessened by exogenous leptin administration (Dong et al., 2013; Landgraf et al., 2014), and hyperleptinemia generates resistance to endotoxemia (Madiehe et al., 2003), improving sepsis survival and modulating the immune response (Siegl et al., 2014). This evidence concerns the gene LEP and serum lipopolysaccharide activity.