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Inflammation

Inflammatory memory is skin deep

Nature Reviews Immunology volume 17, page 731 (2017)Cite this article

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EpSCs reside in the basal layer of the skin epithelium and self-renew or undergo a terminal differentiation programme to maintain epithelial integrity. The authors used an imiquimod (IMQ)-induced model of skin inflammation to explore how EpSCs respond to inflammatory challenges. Topical application of IMQ induced hyperthickening and parakeratosis in the epidermis and this was accompanied by EpSC hyperproliferation and apoptosis, which peaked at day 6 and subsided by day 30. Lineage-tracing experiments showed that EpSCs persisted in the skin in equivalent numbers before, during and after the resolution of inflammation, whereas progenitors that had committed to terminal differentiation were shed. To test whether the inflammatory challenge had a lasting effect on EpSCs, the authors compared wound healing in naive mice and mice that had recovered from IMQ-induced inflammation. Notably, mice previously exposed to inflammation closed their wounds ∼2.5 times faster than naive mice. Enhanced wound healing was also seen when mice were previously exposed to other inflammatory stimuli or infected with the fungal pathogen Candida albicans. Therefore, skin previously exposed to one inflammatory challenge responds faster to an unrelated secondary challenge.

inflammatory memory in a non-immune cell population

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References

  1. Naik, S. et al. Inflammatory memory sensitizes skin epithelial stem cells to tissue damage. Nature http://dx.doi.org/10.1038/nature24271 (2017)

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  1. Yvonne Bordon
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Bordon, Y. Inflammatory memory is skin deep. Nat Rev Immunol 17, 731 (2017). https://doi.org/10.1038/nri.2017.127

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