Bruijnzeel P L, Kuijper P H, Rihs S, Betz S, Warringa R A, Koenderman L
Swiss Institute of Allergy and Asthma Research, Davos-Platz.
J Invest Dermatol. 1993 Feb;100(2):137-42. doi: 10.1111/1523-1747.ep12462781.
Eosinophil granular protein deposits have been demonstrated in lesional atopic dermatitis skin. This suggests active tissue infiltration of eosinophils. To find an explanation for the tissue influx of eosinophils, eosinophil migration was studied in vitro by means of a microchemotaxis assay. Eosinophils from the circulation of patients with atopic dermatitis showed an altered capacity to respond to chemotactic stimuli in vitro compared with eosinophils from healthy donors. Eosinophils from patients with atopic dermatitis had significantly increased migratory responses toward dose ranges of N-formyl-methionyl-leucyl-phenylalanine, neutrophil-activating factor, platelet-activating factor, and platelet factor 4. Eosinophils from normal individuals did not respond to N-formyl-methionyl-leucyl-phenylalanine and neutrophil-activating factor and responded only slightly to platelet factor 4. The migratory responses toward tumor necrosis factor-alpha and complement factor C5a were identical in both groups. Interleukin-5, an eosinophil-selective cytokine, is a strong modulator of the migratory responses to these chemotaxins in eosinophils from normal donors. A migratory response toward N-formyl-methionyl-leucyl-phenylalanine and neutrophil-activating factor was induced by interleukin-5, whereas the migratory response toward platelet-activating factor and platelet factor 4 was markedly potentiated. In contrast, the response to complement fragment C5a was only slightly influenced. Our findings indicate that the increased migratory responsiveness of eosinophils from patients with atopic dermatitis to various chemotaxins reflects in vivo "priming" of eosinophils, presumably by circulating cytokines such as interleukin-5. This in vivo "priming" is not optimal because it can be further potentiated by renewed contact with interleukin-5.
在特应性皮炎皮损处已证实有嗜酸性粒细胞颗粒蛋白沉积。这表明嗜酸性粒细胞有活跃的组织浸润。为了寻找嗜酸性粒细胞向组织内浸润的原因，通过微趋化性分析在体外研究了嗜酸性粒细胞的迁移。与健康供者的嗜酸性粒细胞相比，特应性皮炎患者循环中的嗜酸性粒细胞在体外对趋化刺激的反应能力发生了改变。特应性皮炎患者的嗜酸性粒细胞对N-甲酰甲硫氨酰亮氨酰苯丙氨酸、中性粒细胞激活因子、血小板激活因子和血小板因子4不同剂量范围的迁移反应显著增强。正常个体的嗜酸性粒细胞对N-甲酰甲硫氨酰亮氨酰苯丙氨酸和中性粒细胞激活因子无反应，对血小板因子4仅稍有反应。两组对肿瘤坏死因子-α和补体因子C5a的迁移反应相同。白细胞介素-5是一种嗜酸性粒细胞选择性细胞因子，是正常供者嗜酸性粒细胞对这些趋化因子迁移反应的强调节剂。白细胞介素-5可诱导对N-甲酰甲硫氨酰亮氨酰苯丙氨酸和中性粒细胞激活因子的迁移反应，而对血小板激活因子和血小板因子4的迁移反应则明显增强。相比之下，对补体片段C5a的反应仅受到轻微影响。我们的研究结果表明，特应性皮炎患者的嗜酸性粒细胞对各种趋化因子迁移反应性增加反映了嗜酸性粒细胞在体内的“预激”状态，推测是由白细胞介素-5等循环细胞因子引起的。这种体内“预激”并非最佳状态，因为再次接触白细胞介素-5可使其进一步增强。
