Abstract
The glycerol fermentation of probiotic Staphylococcus epidermidis (S. epidermidis) in the skin microbiome produced butyric acid in vitro at concentrations in the millimolar range. The exposure of dorsal skin of mice to ultraviolet B (UVB) light provoked a significant increased production of pro-inflammatory interleukin (IL)-6 cytokine. Topical application of butyric acid alone or S. epidermidis with glycerol remarkably ameliorated the UVB-induced IL-6 production. In vivo knockdown of short-chain fatty acid receptor 2 (FFAR2) in mouse skin considerably blocked the probiotic effect of S. epidermidis on suppression of UVB-induced IL-6 production. These results demonstrate that butyric acid in the metabolites of fermenting skin probiotic bacteria mediates FFAR2 to modulate the production of pro-inflammatory cytokines induced by UVB.
Highlights
Skin is a fundamental component of the innate immune system, providing a protective barrier against the penetration of microorganisms and preventing environmental damage to the body
We demonstrate that butyric acid, one of the major metabolites produced by S. epidermidis fermentation, attenuates the ultraviolet B (UVB)-induced production of inflammatory cytokines by interacting with cognate receptors expressed by keratinocytes
In rich media incubated with bacteria, the color of phenol red changed from red to orange because of the bacterial replication during incubation
Summary
Skin is a fundamental component of the innate immune system, providing a protective barrier against the penetration of microorganisms and preventing environmental damage to the body. Prolonged exposure of ultraviolet B (UVB) with a wavelength of 280–320 nm is a significant risk factor causing chronic inflammation, DNA damage, and lipid peroxidation in the epidermis [2] Chronic exposure to this cellular stressor commonly results in skin pathologies such as epidermal hyperplasia, erythema, and edema [3]. We demonstrate that butyric acid, one of the major metabolites produced by S. epidermidis fermentation, attenuates the UVB-induced production of inflammatory cytokines by interacting with cognate receptors expressed by keratinocytes. This suggests that manipulation of the S. epidermidis-butyric acid-FFAR2 axis is a potential therapeutic target to protect against skin inflammatory diseases
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