Hydrocortisone reduces both constitutive and UV-elicited release of epidermal thymocyte activating factor (ETAF) by cultured keratinocytes.
Epidermal thymocyte activating factor (ETAF) is spontaneously released into the media by PAM 212 and A 431 cell lines and cultured normal human keratinocytes. ETAF from all 3 cell types can substitute for interleukin 1 (IL-1) in the augmentation of proliferation of a helper T-cell clone (D10.G4.1) induced by mitogen. Hydrocortisone (HC) substantially reduces the release of ETAF by these keratinocytes and, further, appears to induce the release of an inhibitor of lymphocyte activating factor activity of IL-1. Irradiation with UVC causes increased ETAF release into the media. Hydrocortisone abrogates this effect. Thus HC reduces both constitutive and elicited release of ETAF. ETAF plays a major role in inflammation; the ability of HC to block ETAF release by keratinocytes may account for the anti-inflammatory effect of glucocorticosteroids on the skin.
D000818:Animals; D001688:Biological Products / Q000378:metabolism; D002478:Cells, Cultured; D016207:Cytokines; D004817:Epidermis / Q000378:metabolism* / Q000502:physiology; D006854:Hydrocortisone / Q000494:pharmacology*; D007375:Interleukin-1 / Q000037:antagonists & inhibitors / Q000378:metabolism* / Q000494:pharmacology; D051379:Mice; D012636:Secretory Rate / Q000187:drug effects / Q000528:radiation effects; D014466:Ultraviolet Rays
D001688:Biological Products; D016207:Cytokines; D007375:Interleukin-1; D006854:Hydrocortisone