O8 Ultraviolet radiation reshapes the metabolome of skin commensal bacteria, influencing aryl hydrocarbon receptor signalling and barrier function

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ID: 318388
2026
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Abstract
Abstract Introduction and aims Ultraviolet radiation (UVR) is an environmental stressor to the skin and its associated microbiota. Many commensal bacteria produce tryptophan-derived metabolites that modulate epidermal barrier function through aryl hydrocarbon receptor (AhR) signalling. However, the effects of UVR on these metabolic outputs and the subsequent effects on skin barrier function remain unclear. This study examined these interactions. Methods Individual skin commensal bacteria were irradiated with 37.5 mJ cm−2 or 150 mJ cm−2 of solar-simulated radiation (SSR). Cell-free supernatants (CFSNs) were collected and analysed for tryptophan metabolites (using liquid chromatography–mass spectrometry), untargeted metabolites (using gas chromatography–mass spectrometry), and AhR agonist activity (via a reporter assay). The effects on barrier function were assessed by measuring transepithelial electrical resistance (TEER) of CFSN-treated keratinocyte cultures. Time-course expression of tryptophan-related genes after irradiation was measured using quantitative polymerase chain reaction. Results Unirradiated bacterial metabolomes were species-specific. Following irradiation, the abundance of metabolites generated by the indole-pathway generally increased after 37.5mJ but decreased following 150 mJ. Untargeted analyses revealed several decreases in amino and organic acid production after high-dose SSR, while 37.5 mJ resulted in fewer changes. Low-dose SSR upregulated genes involved in tryptophan metabolism (ipdC, ALDH) and synthesis (trpE). AhR agonism increased in 10/12 organisms following irradiation, statistically correlating with increased levels of indole-pathway metabolites (indole-3-acetamide, tryptophol, indole-3-carboxaldehyde, and tryptamine). Keratinocytes treated with irradiated Staphylococcus hominis, Micrococcus luteus and Staphylococcus capitis CFSNs showed enhanced TEER, concurrent with increased AhR activation; inhibiting the AhR removed this effect. Conclusions UVR significantly alters the metabolomes of skin commensal bacteria, with knock-on effects for AhR signalling and barrier integrity, potentially influencing the skin’s response to UVR.
Reference Key
openalex_W7165627652 Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Steven Mercer, Abigail Elias, George Taylor, Geoff Briggs, Mike Bell, Andrew McBain, Catherine O’Neill
Journal the british journal of dermatology
Year 2026
DOI
10.1093/bjd/ljag151.008
URL
https://doi.org/10.1093/bjd/ljag151.008
Keywords Keywords not found

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