IL10 and bacterial infectious disease: M2 macrophages promote angiogenesis and vascular maturation to accelerate tissue repair after pathogen clearance.[43] However, after bacterial infection, the transition from pro‐inflammatory M1 phenotype to anti‐inflammatory M2 phenotype is often delayed.[44] In this study, Que‐Fe‐CeMPF effectively stimulated macrophage polarization toward the “repairing” M2 phenotype by upregulating the anti‐inflammatory cytokine IL‐10 and downregulating pro‐inflammatory cytokines TNF‐α and IL‐6 (Figure 7).