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). This evidence concerns the gene TNF and bacterial infectious disease.