In our research, rTcpC treatment profoundly promoted expression of CD163 and CD206 in THP-1 and J774A.1 and stimulated differentiation into M2 macrophages with IL-4, demonstrating that TcpC promotes M2a macrophage polarization, hereby favoring UPEC to escape from the macrophage-mediated inflammatory anti-infection response. Here, MRC1 is linked to infection.