Busse W W, Lantis S D
J Invest Dermatol. 1979 Aug;73(2):184-7. doi: 10.1111/1523-1747.ep12581674.
Many clinical abnormalities in atopic eczema have been attributed to an imbalance in autonomic nervous system control, specifically a partial blockade of beta-adrenergic responsiveness. The lysosomal enzyme beta-glucuronidase is released from granulocytes during in vitro incubation with complement-activated zymosan particles. Isoproterenol will inhibit the release of this lysosomal enzyme from the granulocyte and the isoproterenol effect is associated with increased granulocyte cyclic AMP formation. In atopic eczema and asthma, this granulocyte response to isoproterenol is impaired. Histamine also inhibits in vitro zymosan induced release of beta-glucuronidase and this is an H2 histamine effect. In asthma, this H2 histamine response is diminished. In the following study, we found a similar impairment in histamine inhibition of beta-glucuronidase release and formation of granulocyte cAMP in atopic eczema. This defect was found only in granulocytes from patients with active eczema. Thus in active atopic eczema, defects in the pharmacological response of the granulocyte are not limited to beta-adrenergic agonists but include H2 histamine activity.
特应性皮炎中的许多临床异常都归因于自主神经系统控制失衡，特别是β-肾上腺素能反应性的部分阻断。溶酶体酶β-葡萄糖醛酸酶在体外与补体激活的酵母聚糖颗粒孵育期间从粒细胞中释放出来。异丙肾上腺素会抑制这种溶酶体酶从粒细胞中的释放，且异丙肾上腺素的作用与粒细胞环磷酸腺苷（cAMP）生成增加有关。在特应性皮炎和哮喘中，粒细胞对异丙肾上腺素的这种反应受损。组胺也会抑制体外酵母聚糖诱导的β-葡萄糖醛酸酶释放，这是一种H2组胺效应。在哮喘中，这种H2组胺反应减弱。在以下研究中，我们发现特应性皮炎中组胺对β-葡萄糖醛酸酶释放的抑制以及粒细胞cAMP生成存在类似的受损情况。这种缺陷仅在活动性湿疹患者的粒细胞中发现。因此，在活动性特应性皮炎中，粒细胞的药理反应缺陷不仅限于β-肾上腺素能激动剂，还包括H2组胺活性。
