Urocanase-Positive Skin-Resident Bacteria Metabolize cis-Urocanic Acid and in Turn Reduce the Immunosuppressive Properties of UVR
Clinical Summary
View sourceWhat was studied
In a mouse model of UVB-induced immunosuppression to the chemical allergen 2,4-dinitrofluorobenzene, the investigators tested whether the UV photoproduct cis-urocanic acid reshapes skin bacteria and alters immune tolerance, using 16S sequencing, in vitro culture, LC-MS, and gnotobiotic-like mice. They also evaluated whether a topical urocanase inhibitor blocks bacterial metabolism of cis-urocanic acid.
Key findings
Acute UVB caused a transient restructuring of skin microbiota via cis-urocanic acid; Staphylococcus epidermidis and other HutU+ bacteria metabolized cis-urocanic acid, proliferated, and lowered its levels, which reduced UVR’s suppression of adaptive immunity and tolerance to 2,4-dinitrofluorobenzene. Topical inhibition of urocanase curtailed this metabolism and restored immunosuppression.
Study limitations
Preclinical mouse model under gnotobiotic-like conditions; no human data or clinical outcomes. Sample size and effect magnitudes were not reported in the abstract.
Clinical implications
This is mechanistic, preclinical evidence: the skin microbiome can blunt UV-induced immunosuppression, and blocking bacterial urocanase restored it in mice. Clinicians should view this as hypothesis-generating; human studies are needed before considering microbiome- or urocanase-targeted approaches to influence phototherapy responses.
Related Questions
Explore related topics and deepen your understanding