However, in mouse models of zymosan-induced peritonitis, lipopolysaccharide-induced acute lung inflammation, and excisional cutaneous skin wounds, the inhibition of endogenous chemerin activity or a loss of ChemR23 expression led to the exacerbation of inflammation and increased leukocyte infiltration, suggesting a protective role in these physiologic contexts [16, 25, 26]. The gene discussed is CMKLR1; the disease is peritonitis.