PTX3 promotes macrophage efferocytosis and inflammation resolution in granulomatous mastitis

infection was applied to establish a rat GM model. Histological analysis showed that the progression of GM was accompanied with the damage of DECs. The serum and mRNA levels and protein expression of PTX3 was increased in GM rat models. PTX3 overexpression drove macrophage to M2 macrophage polarization, inhibiting inflammation response. PTX3 overexpression promoted clearance of apoptotic mammary duct epithelial cells (DECs) by M2 macrophages. However, PTX3 depletion in macrophage inhibited M2 macrophage polarization and impaired the efferocytotic ability, mediating inflammatory response and accumulation of apoptotic DECs. In summary, PTX3 exerts protective function in GM. PTX3-mediated M2 macrophage polarization promotes the clearance of apoptotic DECs. Therefore, targeting the communication between macrophages and DECs may be a promising strategy for GM.