Ruzicka T, Simmet T, Peskar B A, Ring J
J Invest Dermatol. 1986 Feb;86(2):105-8. doi: 10.1111/1523-1747.ep12284061.
Since the biochemical events leading to cutaneous inflammation in atopic dermatitis and psoriasis are unknown, we studied the levels of arachidonic acid-derived mediators of inflammation as well as histamine in the suction blister fluid obtained from lesional and nonlesional skin of patients with these dermatoses. Mediator levels were determined radioimmunologically. Skin from healthy controls and uninvolved skin from patients contained very low or unmeasurable levels of the 5-lipoxygenase metabolite of arachidonic acid, leukotriene (LT) B4. In contrast, higher levels of LTB4-like immunoreactivity were detected in suction blister fluid from lesional atopic dermatitis skin, and even higher concentrations occurred in psoriasis lesions. LTB4-like immunoreactivity from atopic dermatitis suction blister fluid cochromatographed on reverse-phase high-pressure liquid chromatography with authentic LTB4, thus excluding cross-reaction of the LTB4-antibody with arachidonic acid or monohydroxyeicosatetraenoic acids. In contrast, suction blister concentrations of the cyclooxygenase metabolite of arachidonic acid prostaglandin (PG) E2 showed no significant differences between lesional and nonlesional patient skin and healthy control skin. PGD2 determined as a stable metabolite could not be detected in these samples. Histamine concentrations in lesional skin were within normal range. The elevated levels of the potent proinflammatory and immunomodulating mediator LTB4 could be involved in the pathogenesis of cutaneous inflammation in atopic dermatitis and psoriasis. In addition, they might explain the therapeutic efficiency of glucocorticosteroids, which among other actions inhibit the release of arachidonic acid from phospholipid stores by blocking the enzyme phospholipase A2. However, the specificity of disease expression in atopic dermatitis and psoriasis must be due to factors other than cutaneous LTB4 elevation.
由于导致特应性皮炎和银屑病皮肤炎症的生化事件尚不清楚，我们研究了花生四烯酸衍生的炎症介质以及组胺在这些皮肤病患者皮损和非皮损皮肤的吸疱液中的水平。通过放射免疫法测定介质水平。健康对照组的皮肤以及患者的非受累皮肤中，花生四烯酸的5-脂氧合酶代谢产物白三烯（LT）B4的水平非常低或无法检测到。相比之下，在特应性皮炎皮损皮肤的吸疱液中检测到较高水平的LTB4样免疫反应性，而在银屑病皮损中该浓度更高。特应性皮炎吸疱液中的LTB4样免疫反应性在反相高压液相色谱上与纯品LTB4共色谱，从而排除了LTB4抗体与花生四烯酸或单羟基二十碳四烯酸的交叉反应。相比之下，花生四烯酸前列腺素（PG）E2的环氧化酶代谢产物在患者皮损和非皮损皮肤以及健康对照皮肤的吸疱液浓度之间没有显著差异。在这些样本中未检测到作为稳定代谢产物测定的PGD2。皮损皮肤中的组胺浓度在正常范围内。强效促炎和免疫调节介质LTB4水平的升高可能参与了特应性皮炎和银屑病皮肤炎症的发病机制。此外，它们可能解释了糖皮质激素的治疗效果，糖皮质激素除其他作用外，还通过阻断磷脂酶A2来抑制花生四烯酸从磷脂储存中的释放。然而，特应性皮炎和银屑病疾病表现的特异性必定归因于皮肤LTB4升高以外的因素。
