Local cortisol activation is involved in EGF-induced immunosuppression

Dermato-endocrinology
Sayaka MatsumuraIchiro Katayama

Abstract

The major effects of the epidermal growth factor receptor (EGFR) signalling pathway on keratinocytes are cell proliferation, cell differentiation, and wound healing. In addition to these effects, an immunosuppressive effect of EGFR signalling has been reported. However, the precise mechanism of immunosuppression by EGFR signalling is not well understood. In this study, we clarified the involvement of increased local cortisol activation in EGFR signalling-induced immunosuppression in keratinocytes. EGF treatment up-regulated the expression of 11β-hydroxysteroid dehydrogenase 1 (11β-HSD1) and supernatant cortisol levels in a dose-dependent manner in keratinocytes. 11β-HSD1 is an enzyme that catalyses the conversion of cellular hormonally inactive cortisone into active cortisol. qRT-PCR and ELISA assays indicated that EGF significantly decreased tumour necrosis factor α (TNF- α)-induced interleukin-6 (IL-6) expression in keratinocytes. Similarly, 11β-HSD1 overexpression significantly decreased TNF-α-induced IL-6 expression. We evaluated the role of 11β-HSD1 in immunosuppression through EGFR signalling. Blockade of 11β-HSD1 via 11β-HSD1 inhibitor reversed both the expression and production of TNF-α-induced IL-6, which was decreased...Continue Reading

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