The kinetic participation of macrophages is critical for inflammatory resolution and recovery from myocardial infarction (MI),particularly with respect to the transition from the M1 to the M2 phenotype;however,the underlying mechanisms are poorly understood.Here,we found that the deletion of Prostaglandin (PG) D2 receptor subtype 1 (DP1) in macrophages retarded M2 polarization,antiinflammatory cytokine production and resolution in different inflammatory models,including the MI model.