NIH Research Festival
Dysbiosis of the skin microbiota has often been associated with inflammatory skin conditions, such as atopic dermatitis. Given that keratinocytes represent the major cell type which constitutes the epidermis, they are excellent targets for the analysis of host-microbe interactions which occur on the skin. In this study, we analyzed the potential mechanisms of action by which R. mucosa, a skin commensal isolated from a healthy volunteer, protects human primary keratinocytes during infection with S. aureus. Keratinocyte monolayers were co-cultured with S. aureus and R. mucosa, and antimicrobial peptide (AMP) production and cell death were measured. S. aureus alone induced significant cell death as expected. However, co-culture with both R. mucosa and S. aureus had significantly reduced apoptotic and dead cell populations. Additionally, keratinocytes co-cultured with R. mucosa and S. aureus had significantly higher production of the AMP hBD-3, compared to keratinocytes incubated with either species alone; this trend was not observed for other AMPs such as hBD-2, S100A7, S100A9, nor S100A8. Overall, the skin commensal, R. mucosa, appears to provide protection for keratinocytes by boosting AMP production in the presence of pathogens and by ameliorating cell death caused by S. aureus-induced inflammation. The intracellular signaling mechanisms behind these protective effects mediated by R. mucosa will be further investigated.
Scientific Focus Area: Microbiology and Infectious Diseases
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