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Scientists find microbes on the skin of mice promote tissue healing, immunity

Insights may inform wound management techniques

Date:
January 18, 2018
Source:
NIH/National Institute of Allergy and Infectious Diseases
Summary:
Beneficial bacteria on the skin of lab mice work with the animals' immune systems to defend against disease-causing microbes and accelerate wound healing, according to new research. Researchers say untangling similar mechanisms in humans may improve approaches to managing skin wounds and treating other damaged tissues.
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Beneficial bacteria on the skin of lab mice work with the animals' immune systems to defend against disease-causing microbes and accelerate wound healing, according to new research from scientists at the National Institute of Allergy and Infectious Diseases, part of the National Institutes of Health. Researchers say untangling similar mechanisms in humans may improve approaches to managing skin wounds and treating other damaged tissues. The study was published online today in Cell.

Like humans and other mammals, mice are inhabited by large, diverse microbial populations collectively called the microbiome. While the microbiome is believed to have many beneficial functions across several organ systems, little is known about how the immune system responds to these harmless bacteria.

To investigate, NIAID scientists led by Yasmine Belkaid, Ph.D., chief of the Mucosal Immunology Section of NIAID's Laboratory of Parasitic Diseases, observed the reaction of mouse immune cells to Staphylococcus epidermidis, a bacterium regularly found on human skin that does not normally cause disease. To their surprise, immune cells recognized S. epidermidis using evolutionarily ancient molecules called non-classical MHC molecules, which led to the production of unusual T cells with genes associated with tissue healing and antimicrobial defense. In contrast, immune cells recognize disease-causing bacteria with classical MHC molecules, which lead to the production of T cells that stoke inflammation.

Researchers then took skin biopsies from two groups of mice -- one group that had been colonized by S. epidermidis and another that had not. Over five days, the group that had been exposed to the beneficial bacteria experienced more tissue repair at the wound site and less evidence of inflammation. Dr. Belkaid's team plans to next probe whether non-classical MHC molecules recognize friendly microbes on the skin of other mammals, including humans, and similarly benefit tissue repair. Eventually, mimicking the processes initiated by the microbiome may allow clinicians to accelerate wound healing and prevent dangerous infections, the researchers note.


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Materials provided by NIH/National Institute of Allergy and Infectious Diseases. Note: Content may be edited for style and length.


Journal Reference:

  1. Jonathan L. Linehan, Oliver J. Harrison, Seong-Ji Han, Allyson L. Byrd, Ivan Vujkovic-Cvijin, Alejandro V. Villarino, Shurjo K. Sen, Jahangheer Shaik, Margery Smelkinson, Samira Tamoutounour, Nicholas Collins, Nicolas Bouladoux, Amiran Dzutsev, Stephan P. Rosshart, Jesse H. Arbuckle, Chyung-Ru Wang, Thomas M. Kristie, Barbara Rehermann, Giorgio Trinchieri, Jason M. Brenchley, John J. O’Shea, Yasmine Belkaid. Non-classical Immunity Controls Microbiota Impact on Skin Immunity and Tissue Repair. Cell, 2018; DOI: 10.1016/j.cell.2017.12.033

Cite This Page:

NIH/National Institute of Allergy and Infectious Diseases. "Scientists find microbes on the skin of mice promote tissue healing, immunity." ScienceDaily. ScienceDaily, 18 January 2018. <www.sciencedaily.com/releases/2018/01/180118142618.htm>.
NIH/National Institute of Allergy and Infectious Diseases. (2018, January 18). Scientists find microbes on the skin of mice promote tissue healing, immunity. ScienceDaily. Retrieved March 18, 2024 from www.sciencedaily.com/releases/2018/01/180118142618.htm
NIH/National Institute of Allergy and Infectious Diseases. "Scientists find microbes on the skin of mice promote tissue healing, immunity." ScienceDaily. www.sciencedaily.com/releases/2018/01/180118142618.htm (accessed March 18, 2024).

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