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Oncostatin M (OSM) has been reported to be overexpressed in psoriasis skin lesions and to exert proinflammatory effects in vitro on human keratinocytes. Here, we report the proinflammatory role of OSM in vivo in a mouse model of skin inflammation induced by intradermal injection of murine OSM-encoding adenovirus (AdOSM) and compare with that induced by IL-6 injection. Here, we show that OSM potently regulates the expression of genes involved in skin inflammation and epidermal differentiation in murine primary keratinocytes. In vivo, intradermal injection of AdOSM in mouse ears provoked robust skin inflammation with epidermal thickening and keratinocyte proliferation, while minimal effect was observed after AdIL-6 injection. OSM overexpression in the skin increased the expression of the S100A8/9 antimicrobial peptides, CXCL3, CCL2, CCL5, CCL20, and Th1/Th2 cytokines, in correlation with neutrophil and macrophage infiltration. In contrast, OSM downregulated the expression of epidermal differentiation genes, such as cytokeratin-10 or filaggrin. Collectively, these results support the proinflammatory role of OSM when it is overexpressed in the skin. However, OSM expression was not required in the murine model of psoriasis induced by topical application of imiquimod, as demonstrated by the inflammatory phenotype of OSM-deficient mice or wild-type mice treated with anti-OSM antibodies.

Original publication




Journal article


European journal of immunology

Publication Date





1737 - 1751


Laboratoire Inflammation, Tissus Epithéliaux et Cytokines (LITEC), EA 4331, Université de Poitiers, Poitiers, France.


Epidermis, Keratinocytes, Skin, Animals, Mice, Knockout, Mice, Psoriasis, Disease Models, Animal, Aminoquinolines, Cell Differentiation, Cell Proliferation, Gene Expression, Gene Expression Regulation, Phenotype, Male, Oncostatin M, Biomarkers, Imiquimod, Filaggrin Proteins