Ultraviolet irradiation downregulates the IL-1 receptor in Pam 212 keratinocytes.
There is increasing evidence that keratinocytes, by virtue of production of cytokines, may participate in inflammatory and immune responses in the skin. The expression of keratinocyte cytokines can be modulated by various exogenous and endogenous agents, including ultraviolet light (UV) and cytokines themselves. We have recently shown that augmentation of GM-CSF expression by UVB irradiation is mediated by UV-induced IL-1 in Pam 212 keratinocytes. This may suggest that an autocrine mechanism exists in this murine keratinocyte cell line. In order to further clarify the mechanism by which UV irradiation augments GM-CSF, this study was undertaken to assess the effect of UV on the expression of IL-1 receptor (IL-1R) in Pam 212 keratinocytes. UVB irradiation (35 or 70 J/m2) significantly downregulates the expression of IL-1R mRNA. IL-1R mRNA remains downregulated for 12h after UV, then slowly returns to the steady state level by 24h to 32h after UV. On the other hand, UV augments IL-1 mRNA in a biphasic pattern with an initial phase (by 6h after UV) and a late phase (24h and 48h after UV). The results of these studies indicate that modulation of IL-1R and IL-1 itself by UVB irradiation are important in mediating autocrine cytokine networks in keratinocytes.
Nozaki
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S
Department of Dermatology, Showa University, Tokyo, Japan.
Sauder
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DN
D015536:Down-Regulation; D006801:Humans; D015603:Keratinocytes / Q000378:metabolism*; D012333:RNA, Messenger / Q000378:metabolism; D017472:Receptors, Interleukin-1 / Q000528:radiation effects*; D014466:Ultraviolet Rays
D012333:RNA, Messenger; D017472:Receptors, Interleukin-1