Dooper M W, Timmermans A, Aalbers R, Weersink E J, de Monchy J G, Kauffman H F
Department of Allergology, State University Hospital Groningen, The Netherlands.
Ann Allergy Asthma Immunol. 1995 Mar;74(3):248-54.
Enhanced activities of peripheral blood cells are a common characteristic of patients with asthma.
Here we tested whether this could be due to a dysfunction in one or more signal transduction systems.
The production of 1,2-diacylglycerol (1,2-DAG) and arachidonic acid was compared in mononuclear blood cells from patients with asthma (n = 10) and healthy controls (n = 12).
Using three different stimuli (concanavalin A, aluminium fluoride or the calcium ionophore A23187) no difference in the production of both 1,2-DAG and arachidonic acid could be found between patients and controls before allergen challenge. Concanavalin A-induced 1,2-DAG production could be inhibited completely in the presence of isoprenaline; concanavalin A-induced arachidonic acid production, partially. The inhibitory effect of adenylate cyclase activation on the production of 1,2-DAG and arachidonic acid was identical in patients and controls. Following allergen challenge, there was a tendency to an increased production of 1,2-DAG and arachidonic acid in controls, whereas in patients there was a tendency to a decreased production.
Enhanced cellular activities found in patients with asthma are not caused by an intrinsic dysfunction in production of 1,2-DAG and arachidonic acid.
外周血细胞活性增强是哮喘患者的一个常见特征。
在此我们测试了这是否可能是由于一个或多个信号转导系统功能障碍所致。
比较了哮喘患者（n = 10）和健康对照者（n = 12）外周血单个核细胞中1,2 -二酰甘油（1,2 - DAG）和花生四烯酸的生成情况。
在过敏原激发前，使用三种不同刺激物（刀豆球蛋白A、氟化铝或钙离子载体A23187），患者和对照者之间1,2 - DAG和花生四烯酸的生成均未发现差异。在异丙肾上腺素存在的情况下，刀豆球蛋白A诱导的1,2 - DAG生成可被完全抑制；刀豆球蛋白A诱导的花生四烯酸生成可被部分抑制。腺苷酸环化酶激活对1,2 - DAG和花生四烯酸生成的抑制作用在患者和对照者中是相同的。过敏原激发后，对照者中1,2 - DAG和花生四烯酸的生成有增加趋势，而患者中则有减少趋势。
哮喘患者中发现的细胞活性增强并非由1,2 - DAG和花生四烯酸生成的内在功能障碍引起。
