,52 Additionally, TNF-α/TNFR1- and CXCL1-dependent signaling pathways are important for leptin-induced neutrophil migration in vivo.53 Leptin is also capable of blunting the exacerbated pro-inflammatory cytokine (IL-1β , IL-6, TNF-α) and tissue damage response during endotoxemia, where leptin-deficient mice are more susceptible to LPS-induced death.54 Here, LEP is linked to serum lipopolysaccharide activity.