Journal article
The commensal skin microbiota triggers type I IFN-dependent innate repair responses in injured skin.
- Di Domizio J Department of Dermatology, CHUV University Hospital, University of Lausanne, Lausanne, Switzerland.
- Belkhodja C Department of Dermatology, CHUV University Hospital, University of Lausanne, Lausanne, Switzerland.
- Chenuet P Laboratory of Experimental and Molecular Immunology and Neurogenetics, UMR 7355 CNRS-University of Orleans, Orleans, France.
- Fries A Department of Dermatology, CHUV University Hospital, University of Lausanne, Lausanne, Switzerland.
- Murray T Department of Oncology, CHUV University Hospital, University of Lausanne, Lausanne, Switzerland.
- Mondéjar PM Department of Oncology, CHUV University Hospital, University of Lausanne, Lausanne, Switzerland.
- Demaria O Department of Dermatology, CHUV University Hospital, University of Lausanne, Lausanne, Switzerland.
- Conrad C Department of Dermatology, CHUV University Hospital, University of Lausanne, Lausanne, Switzerland.
- Homey B Department of Dermatology, Medical Faculty, Heinrich-Heine-University, Duesseldorf, Germany.
- Werner S ETH Zurich, Institute of Molecular Health Sciences, Zurich, Switzerland.
- Speiser DE Department of Oncology, CHUV University Hospital, University of Lausanne, Lausanne, Switzerland.
- Ryffel B Laboratory of Experimental and Molecular Immunology and Neurogenetics, UMR 7355 CNRS-University of Orleans, Orleans, France.
- Gilliet M Department of Dermatology, CHUV University Hospital, University of Lausanne, Lausanne, Switzerland. Michel.gilliet@chuv.ch.
- 2020-07-15
Published in:
- Nature immunology. - 2020
English
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.
- Language
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- English
- Open access status
- closed
- Identifiers
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- DOI 10.1038/s41590-020-0721-6
- PMID 32661363
- Persistent URL
- https://sonar.ch/global/documents/185335
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