Ruzicka T, Przybilla B
Department of Dermatology, University of Munich, FRG.
Skin Pharmacol. 1988;1(3):186-91. doi: 10.1159/000210772.
The biochemical basis of ultraviolet-induced cutaneous inflammation in polymorphous light eruption (PLE) is not known. We investigated the potential role of eicosanoids--derivatives of arachidonic acid--as mediators of inflammation in this common disorder. 13 patients were investigated, in whom skin lesions could be experimentally reproduced by repeated UV-A but not UV-B irradiation. Peripheral blood leukocytes of these patients were irradiated with UV-A or UV-B, and the release of leukotriene B4 (LTB4), LTC4 and prostaglandin E2 (PGE2) was measured. Cells from PLE patients, but not healthy controls, released selectively high amounts of LTB4 in response to UV-A. The UV-A-induced LTB4 release was light-dose-dependent. This phenomenon was not observed with UV-B. The selective UV-A-induced release of LTB4 could play a major role in the pathophysiology of cutaneous inflammation in PLE.
多形性日光疹（PLE）中紫外线诱发皮肤炎症的生化基础尚不清楚。我们研究了类花生酸（花生四烯酸的衍生物）作为这种常见疾病炎症介质的潜在作用。对13例患者进行了研究，这些患者的皮肤损伤可通过重复紫外线A（UV-A）照射而非紫外线B（UV-B）照射进行实验性再现。对这些患者的外周血白细胞进行UV-A或UV-B照射，并测量白三烯B4（LTB4）、LTC4和前列腺素E2（PGE2）的释放量。与健康对照不同，PLE患者的细胞在受到UV-A照射后选择性地释放大量LTB4。UV-A诱导的LTB4释放呈光剂量依赖性。UV-B照射未观察到这种现象。UV-A诱导的LTB4选择性释放可能在PLE皮肤炎症的病理生理学中起主要作用。
