Epidermal Cell-Polymorphonuclear Leukocyte Cooperation in the Formation of Leukotriene B4 by Transcellular Biosynthesis
Since 1974 (1) there have been numerous reports in the literature showing the presence of large amounts of eicosanoids in psoriatic lesions. The metabolic pathways of arachidonic acid (AA) in freshly isolated human epidermal cells (EC) are still controversial (2–4). Although it has been reported that human EC can synthesize leukotriene B4 (LTB4) from AA (4), the actual cellular origin of LTB4 found in psoriatic lesions has not been definitively established yet. Infiltration of polymorphonuclear leukocytes (PMN) is one of the earliest events in the pathogenesis of psoriatic lesions and their accumulation can precede the appearance of the characteristic epidermal changes (5, 6). The conversion of PMN-produced leukotriene A4 (LTA4) to LTB4 by EC could contribute to increase the amount of LTB4 present in lesions of psoriasis or other inflammatory dermatoses. In this study, we explore the capability of EC to synthesize LTB4 from AA and/or transform PMN-derived LTA4 into LTB4.
KeywordsArachidonic Acid Epidermal Cell Polymorphonuclear Leukocyte Cold Methanol Psoriatic Lesion
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