Oestrogen inhibits psoriasis-like dermatitis induced by imiquimod in mice in relation to increased IL-10 producing cells despite elevated expression of IL-22, IL-23, IL-17 mRNA

Sex hormones influence the development and natural course of psoriasis. Here, we examined the effects of female sex hormones, particularly oestrogen, on psoriasis-like dermatitis induced using topical imiquimod in mice that underwent either sham operation (Sham) or ovariectomy (OVX), with (hormone replacement treatment: HRT) or without 17 beta-oestradiol targeting the maximum physiological levels. The number of neutrophils in the skin was higher in the order of OVX-, Sham-, and HRT-treated mice. However, no significant difference was detected in the clinical scores among the three groups due to severe erythema and scale in a few mice out of HRT-treated mice in a set of experiments. OVX- and HRT-treated mice showed increased mRNA levels of interleukin (IL)-22 and IL-23 compared with Sham-treated mice; increased IL-10 mRNA levels were found in HRT-treated mice, possibly due to an increased proportion of forkhead box P3 (Foxp3)- and IL-10 positive large cells (possibly macrophages). In addition, HRT-treated mice had a more compact stratum corneum with higher expression of loricrin and involucrin than OVX- and Sham-treated mice. This study suggests that oestrogen has a dual potential in the pathogenesis of psoriasis: suppression of inflammation by enhancing IL-10 production and enhancement of inflammation by induction of IL-22 and IL-23 expression.

Automated summary

Sex hormones, particularly estrogen, have dual effects on the pathogenesis of psoriasis. Estrogen can suppress inflammation by enhancing IL-10 production, but can also enhance inflammation by inducing IL-22 and IL-23 expression.