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Skin commensal bacteria Staphylococcus epidermidis promote survival of melanocytes bearing UVB ‐induced DNA damage, while bacteria Propionibacterium acnes inhibit survival of melanocytes by increasing apoptosis
Author(s) -
Wang Zhenping,
Choi JaeEun,
Wu ChiaChi,
Di Nardo Anna
Publication year - 2018
Publication title -
photodermatology, photoimmunology and photomedicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.736
H-Index - 60
eISSN - 1600-0781
pISSN - 0905-4383
DOI - 10.1111/phpp.12411
Subject(s) - propionibacterium acnes , staphylococcus epidermidis , biology , microbiology and biotechnology , dna damage , commensalism , human skin , bacteria , apoptosis , flow cytometry , immunology , dna , staphylococcus aureus , biochemistry , genetics
Summary Background/Purpose Skin commensal bacteria have been described to help orchestrate skin homeostasis, signaling through innate immunity pathways. This study for the first time aimed at studying the relationship between skin commensals and melanocytes after UVB exposure. Methods An in vitro UVB radiation model with normal human epidermal melanocytes ( NHM s) and skin commensal bacteria supernatant from Staphylococcus epidermidis and Propionibacterium acnes was established. Melanocytes DNA damage, cyclobutane pyrimidine dimers ( CPD ), and cellular proliferation marker Ki‐67 were measured by ELISA and immunofluorescence staining. Cell apoptosis was assessed by flow cytometry and PCR array and RT ‐ qPCR . Results Normal human epidermal melanocytes are able to survive and proliferate while bearing DNA damage after UVB radiation. Skin commensal bacteria S. epidermidis and its by‐product LTA promote melanocytes survival by inducing upregulation of TRAF 1, CASP 14, CASP 5, and TP 73. On the other hand, P. acnes can inhibit UVB ‐irradiated melanocytes survival by increasing apoptosis. Conclusion Our studies show different aspects of commensal activity on melanocytes during irradiation. The possible balance achieved by the different skin commensal can influence NHM potential to become cancer cells.