Bcl-3 expression in the imiquimod-induced psoriasis mouse skin.

OBJECTIVE

Psoriasis is an inflammatory process in the skin involving the loss of normal function of immune cells and keratinocytes. TNF-α is a pro-inflammatory cytokine involved in psoriasis induced by NF-κB activation. In contrast, the anti-inflammatory cytokine IL-10 can suppress macrophage TNF-α production. The non-classical NF-κB regulator, Bcl-3, can regulate IL-10 expression. Limited knowledge exists on Bcl-3 and IL-10 expression in psoriasis and their action on TNF-α. This study evaluated Bcl-3, TNF-α, and IL-10 expression levels in mouse skin in a model of imiquimod-induced psoriasis.

RESULTS

Female Balb/c mice were shaved in the lumbar region and administered 62 mg of 5% imiquimod (IMQ) cream for six consecutive days. The non-lesional group received only 62 mg of cream without IMQ for six consecutive days. RT-qPCR was used to determine Bcl-3, TNF-α, and IL-10 expression. Imiquimod psoriasis induction was confirmed phenotypically and histologically. On day 2 of imiquimod treatment, the lesioned skin significantly reduced the expression level of Bcl-3, and TNF-α. However, on day 6, a significant difference in the expression of Bcl-3 (sixfold), TNF-α (twofold), and IL-10 (threefold) was found in lesioned skin compared to non-lesioned skin. Results suggest that late-stage overexpression of Bcl-3 in lesioned skin induces IL-10 expression to regulate TNF-α inflammatory effects.