Editors' ChoiceWound Healing

Time to ditch topical antibiotics?

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Science Signaling  01 Jun 2021:
Vol. 14, Issue 685, eabj6974
DOI: 10.1126/scisignal.abj6974

Commensals promote skin regeneration and wound healing by stimulating IL-1β signaling in keratinocytes.

Commensal microbes protect the skin from pathogens and promote its epithelial barrier function. They also stimulate re-epithelialization of wounds and shape adaptive immunity through T cell–dependent mechanisms (see Gonzalez et al.). Wang et al. now report that commensal bacteria stimulate skin regeneration through innate immune responses. Unlike superficial skin wounds, full-thickness skin wounds in mice trigger the regeneration of stem cell pools, nerves, and structures such as hair follicles and sebaceous glands, a phenomenon known as wound-induced hair neogenesis (WIHN). The authors found that reducing or eliminating skin commensals slowed WIHN and reduced the expression of skin stem cell markers in wounds. The commensal species Staphylococcus epidermidis—and even the opportunistic pathogen S. aureus—stimulated WIHN when injected into wounds. Bacteria-induced WIHN depended on the inflammatory cytokine interleukin-1β (IL-1β), which was produced by both keratinocytes and macrophages in the wound bed, and on MyD88-mediated signaling through the receptor IL-1R specifically in keratinocytes. IL-1β also stimulated the expression of stem cell markers in cultured human keratinocytes. WIHN has not been proven to occur in humans, but an over-the-counter, broad-spectrum antibiotic ointment commonly used on skin wounds delayed wound closure and reduced the expression of inflammatory and healing-associated markers in human subjects. As in mice, wound closure in human subjects also correlated with the presence of S. aureus, suggesting that wound healing benefits from even potentially pathogenic skin bacteria.

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