Pentland A P, Mahoney M G
Division of Dermatology, Washington University School of Medicine, St. Louis, Missouri 63110.
J Invest Dermatol. 1990 Jan;94(1):43-6. doi: 10.1111/1523-1747.ep12873337.
Keratinocytes are a rich source of IL-1, a cytokine which stimulates prostaglandin synthesis in many cell types. The effects on arachidonic acid metabolism of this cytokine were therefore studied in cultured adult human keratinocytes. Exogenous IL-1 increased basal cellular prostaglandin synthesis (particularly PGE2) threefold. Increased PGE2 synthesis in response to IL-1 was inhibited by cycloheximide, suggesting a requirement for new protein synthesis. Irradiation of the keratinocytes with low-dose ultraviolet light B (UVB) resulted in the release of increased quantities of both IL-1 and PGE2. The amount of IL-1 released was sufficient to increase PGE2 synthesis when exogenously added to unstimulated cells, suggesting a causal relationship. The time course of accumulation of IL-1 and PGE2 in the medium of irradiated keratinocytes was also consistent with a cause-effect relationship. No feedback inhibition of IL-1 release by the increased PGE2 was detected as demonstrated by the observation that IL-1 production in response to UVB was not augmented by treatment with indomethacin or blunted by the exogenous addition of PGE2. These data suggest that keratinocyte IL-1 may be partially responsible for induction of keratinocyte PGE2 synthesis after UVB irradiation.
角质形成细胞是白细胞介素-1（IL-1）的丰富来源，IL-1是一种能刺激多种细胞类型中前列腺素合成的细胞因子。因此，在培养的成人角质形成细胞中研究了这种细胞因子对花生四烯酸代谢的影响。外源性IL-1使基础细胞前列腺素合成（尤其是PGE2）增加了三倍。环己酰亚胺抑制了因IL-1导致的PGE2合成增加，这表明需要新的蛋白质合成。用低剂量紫外线B（UVB）照射角质形成细胞会导致IL-1和PGE2释放量增加。当外源性添加到未受刺激的细胞中时，释放的IL-1量足以增加PGE2合成，这表明存在因果关系。照射后的角质形成细胞培养基中IL-1和PGE2积累的时间进程也与因果关系一致。如观察到用吲哚美辛处理不会增强UVB诱导的IL-1产生，外源性添加PGE2也不会使其减弱，这表明未检测到增加的PGE2对IL-1释放的反馈抑制。这些数据表明，角质形成细胞IL-1可能部分负责UVB照射后角质形成细胞PGE2合成的诱导。
