Skin wounds heal by coordinated induction of inflammation and tissue repair, but the initiating events are poorly defined. Here we uncover a fundamental role of commensal skin microbiota in this process and show that it is mediated by the recruitment and the activation of type I interferon (IFN)-producing plasmacytoid DC (pDC). Commensal bacteria colonizing skin wounds trigger activation of neutrophils to express the chemokine CXCL10, which recruits pDC and acts as an antimicrobial protein to kill exposed microbiota, leading to the formation of CXCL10–bacterial DNA complexes. These complexes and not complexes with host-derived DNA activate pDC to produce type I IFNs, which accelerate wound closure by triggering skin inflammation and early T cell–independent wound repair responses, mediated by macrophages and fibroblasts that produce major growth factors required for healing. These findings identify a key function of commensal microbiota in driving a central innate wound healing response of the skin.

皮肤伤口通过炎症和组织修复的协同诱导而愈合，但是起始事件的定义不明确。在这里，我们揭示了共生皮肤微生物群在此过程中的基本作用，并表明它是由募集和激活产生I型干扰素（IFN）的浆细胞样DC（pDC）介导的。侵染皮肤伤口的共生细菌触发中性粒细胞的活化，以表达趋化因子CXCL10，后者吸收pDC并作为杀灭暴露的微生物群的抗菌蛋白，导致形成CXCL10-细菌DNA复合物。这些与宿主来源的DNA形成的复合物（而非复合物）激活pDC以产生I型干扰素，从而通过触发皮肤炎症和早期T细胞非依赖性伤口修复反应来加速伤口闭合，由巨噬细胞和成纤维细胞介导，可产生愈合所需的主要生长因子。这些发现确定了共生菌群在驱动皮肤中枢先天性伤口愈合反应中的关键功能。