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BackgroundA relationship between alcohol consumption and psoriasis has been reported, but it is unclear whether alcohol consumption aggravates psoriasis. Here, we studied the effect of chronic ethanol (EtOH) consumption in the murine model of Aldara-induced psoriasiform dermatitis.MethodsC57BL/6 mice received 5% EtOH in their drinking water for 10 weeks. Dermatitis was induced from weeks 9 to 10, by applying Aldara to the shaved patch of skin on the back. Inflammation was characterized by histological and transcriptomic analyses.ResultsEtOH consumption aggravated Aldara-induced dermatitis. The scales were more severe, epidermal thickening was more pronounced, and cutaneous expression of Th17-related cytokines was exacerbated. Control mice simply receiving EtOH displayed minimal cutaneous inflammation, characterized by epidermal infiltrates of T lymphocytes and the overexpression of IL-17A and the Th17-recruiting chemokine CCL20. In vitro studies showed that low concentrations of EtOH induce the expression of CCL20 by murine epidermal keratinocytes.ConclusionAlcohol consumption leads to subliminar skin inflammation, which is revealed by the exacerbation of Aldara-induced experimental psoriasiform dermatitis, likely through Th17-type minimal skin inflammation. These results favor the systematic management of alcohol consumption in psoriatic patients.

Original publication




Journal article


Alcoholism, clinical and experimental research

Publication Date





1728 - 1733


From the, Laboratoire Inflammation Tissus Epithéliaux et Cytokines EA 4331, (PV, MP, CG, J-FJ, FM, CS, J-CL), Université de Poitiers, Poitiers, France.


Keratinocytes, Skin, Animals, Mice, Psoriasis, Ethanol, Central Nervous System Depressants, Interleukins, Interleukin-17, Interferon Inducers, Gene Expression Profiling, Alcohol Drinking, Interleukin-23, Chemokine CCL20, Th17 Cells, Imiquimod