Abstract
BackgroundSkin resident microbial species are often thought of either as pathogenic or commensal. However, little is known about the role of the skin barrier in modulating their potential for causing disease. To investigate this question we measured the effects of three microbial species commonly found on the skin (Staphylococcus epidermidis, Staphylococcus aureus, and Propionibacterium acnes) on a reconstructed human epidermal model by either applying the bacteria on the model surface (intact barrier) or adding them to the culture medium (simulating barrier breach).ResultsWhen added to the medium, all of the tested species induced inflammatory responses and keratinocyte cell death with species-specific potency. P. acnes and S. epidermidis induced specific alterations in the expression of keratinocyte differentiation and proliferation markers, suggesting a barrier reparation response. S. aureus induced complete keratinocyte cell death. On the contrary, topically applied S. epidermidis and P. acnes caused no inflammatory response even when tested at high concentrations, while topical S. aureus induced a weak reaction. None of the tested species were able to alter the expression of keratinocyte differentiation or expression markers, when applied topically.ConclusionsWe show that the skin barrier prevents the effects of common skin bacteria on epidermal keratinocyte inflammation, differentiation and proliferation and highlight the importance of skin barrier in defending against the pathogenic effects of common skin bacteria.
Highlights
Skin resident microbial species are often thought of either as pathogenic or commensal
Effects of bacteria added in the medium on keratinocyte inflammation and viability We tested the effects of bacteria added to the Reconstructed Human Epidermis (RHE) medium, essentially underneath the RHE keratinocytes in order to mimic a scenario in which the bacteria had penetrated the epidermal barrier
S. aureus was the most cytotoxic and pro-inflammatory of the species added to the RHE medium and stimulated a large and statistically significant increase in Interleukin 1-alpha (IL-1α) and Lactate Dehydrogenase (LDH) release when added at just 1 × 107 Colony Forming Units (CFU) (Figure 2)
Summary
Skin resident microbial species are often thought of either as pathogenic or commensal. Little is known about the role of the skin barrier in modulating their potential for causing disease. To investigate this question we measured the effects of three microbial species commonly found on the skin (Staphylococcus epidermidis, Staphylococcus aureus, and Propionibacterium acnes) on a reconstructed human epidermal model by either applying the bacteria on the model surface (intact barrier) or adding them to the culture medium (simulating barrier breach). Staphylococcus epidermidis, the most common cutaneous bacteria, secretes antimicrobial phenol-soluble modulins [4], while stimulating secretion of antimicrobial peptides from keratinocytes, providing increased resistance to pathogen infection [5]. It could be expected that the skin adjusts its physiological conditions to favor colonization by commensal microflora species over pathogenic species during this period
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