 In any event, combined disruption of the "Fpr2" and "Fpr3" genes causes mice to mount enhanced acute inflammatory responses as evidenced in three models, intestine inflammation caused by mesenteric artery ischemia-reperfusion, paw swelling caused by carrageenan injection, and arthritis caused by the intraperatoneal injection of arthritis-inducing serum.Since "Fpr2" gene knockout mice exhibit a faulty innate immune response to intravenous "listeria monocytogenes" injection, these results suggest that the human FPR2 receptor and mouse Fpr3 receptor have equivalent functions in dampening at least certain inflammatory response.Rats express an ortholog of FPR2 (74% amino acid sequence identity) with high affinity for lipoxin A4.