Decoding the Complexity of Delayed Wound Healing Following Enterococcus Faecalis Infection

The study investigates the impact of Enterococcus faecalis on wound healing using single-cell RNA sequencing in a mouse model, analyzing over 23,000 cells. The findings reveal that E. faecalis infection leads to unique transcriptional and metabolic changes, particularly in keratinocytes and fibroblasts, creating an anti-inflammatory environment. The infection causes a premature and incomplete epithelial-mesenchymal transition in keratinocytes and modulates M2-like macrophage polarization, inhibiting pro-inflammatory resolution. Additionally, macrophage-neutrophil crosstalk regulates chemokine signaling and promotes anti-inflammatory interactions with endothelial cells. These insights highlight the immunosuppressive role of E. faecalis in delaying wound healing.