Transmissible Dysbiotic Skin Microbiota that Promotes Skin Inflammation

Cutaneous Leishmaniasis causes skin microbiome dysbiosis which could be transferred between infected and uninfected mice.

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Jul 05, 2017
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New research from Elisabeth Grice and Phillip Scott at the University of Pennsylvania has shown that dysbiosis in the skin of lab mice was transimissible and promoted higher levels of skin inflammation.

The team began in vivo experiments after discovering a trend in the microbiome of Leishmania infected individuals in Brazil with the help of their collaborators at Universidade Federal da Bahia. The saw that infected people had dysbiotic microbiomes with reduced diversity which were dominated by staphylococci and streptococci. 

This finding was mirrored in a mouse model. What was surprising was that the dysbiotic microbiome could be transferred to uninfected mice sharing the same cage. The uninfected mice then showed increased inflammation and when they were eventually infected with L. major, had much worse symptoms. 

This is bound to have implications in the future although it is not clear what they are. A dysibiotic microbiome could become a marker for an underlying infection or even an early warning sign. If dysbiotic skin microbiomes can be transferred, it may be possible to transfer healthy microbiomes to reduced inflammation and the risk of infection.

Highlights

  • Leishmania infection alters the skin microbiota of both humans and mice
  • Dysbiosis is characterized by a dominance of Staphylococcus and/or Streptococcus
  • Naive mice acquire dysbiosis when co-housed with leishmania-infected mice
  • Acquiring a dysbiotic microbiota prior to infection exacerbates skin inflammation

Summary

Skin microbiota can impact allergic and autoimmune responses, wound healing, and anti-microbial defense. We investigated the role of skin microbiota in cutaneous leishmaniasis and found that human patients infected with Leishmania braziliensis develop dysbiotic skin microbiota, characterized by increases in the abundance of Staphylococcus and/or Streptococcus. Mice infected with L. major exhibit similar changes depending upon disease severity. Importantly, this dysbiosis is not limited to the lesion site, but is transmissible to normal skin distant from the infection site and to skin from co-housed naive mice. This observation allowed us to test whether a pre-existing dysbiotic skin microbiota influences disease, and we found that challenging dysbiotic naive mice with L. major or testing for contact hypersensitivity results in exacerbated skin inflammatory responses. These findings demonstrate that a dysbiotic skin microbiota is not only a consequence of tissue stress, but also enhances inflammation, which has implications for many inflammatory cutaneous diseases.

Reference

Gimblet et al., Cutaneous Leishmaniasis Induces a Transmissible Dysbiotic Skin Microbiota that Promotes SkinInflammation, Cell Host & Microbe (2017), http://dx.doi.org/10.1016/j.ch...

Go to the profile of Ben Libberton

Ben Libberton

Communications Officer, MAX IV Laboratory

I'm a Communications Officer at MAX IV Laboratory in Lund, Sweden and the Community Editor for npj Biofilms and Microbiomes. I'm interested in how bacteria cause disease and look to technology to produce novel tools to study and ultimately prevent infection. Part of my current role is to find ways to use synchrotron radiation to study microorganisms.

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