哮喘患者肺泡巨噬细胞中paf-乙醚和β -葡糖醛酸酶的抗原释放。

B Arnoux, M Joseph, M H Simoes, A B Tonnel, P Duroux, A Capron, J Benveniste
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引用次数: 0

摘要

比较对照组(n = 12)和特应性患者(n = 19,未治疗12,茶碱治疗4,茶碱和皮质类固醇治疗3)肺泡巨噬细胞(AM)释放介质的能力。AM通过2小时的粘附纯化,并用普遍过敏原、特异性致敏过敏原、抗igg或抗ige血清攻毒。测定paf-乙醚、lyso paf-乙醚和β -葡糖醛酸酶的释放量。研究了paf -醚及其lyso衍生物在洗净兔血小板中的作用。在未经治疗的特应性患者的AM特异性致敏或抗ige血清刺激后获得酶和介质释放。体外免疫刺激后,AM、对照组和治疗组均未检测到paf-acether的释放,而治疗组和治疗组的lyso paf-acether的释放均大大降低。对照患者被动致敏后,经免疫激发AM获得释放。AM释放具有支气管收缩活性的介质可能是人类哮喘的另一种病因途径。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Antigenic release of paf-acether and beta-glucuronidase from alveolar macrophages of asthmatics.

Alveolar macrophages (AM) from control (n = 12) and atopic patients (n = 19, 12 without treatment, 4 treated with theophylline and 3 with theophylline and corticosteroid) were compared for their capacity to release mediators. AM were purified by 2 h adherence and challenged with either ubiquitous allergen, specific sensitizing allergens, anti-IgG or anti-IgE serum. The release of paf-acether, lyso paf-acether and beta-glucuronidase was measured. Paf-acether and its lyso derivative were assayed on washed rabbit platelets. Enzyme and mediator releases were obtained after specific allergenic or anti-IgE serum challenge of AM from untreated atopic patients. No release of paf-acether was detected from AM, from control or treated atopic patients after in vitro immunological challenge, whereas that of lyso paf-acether was greatly reduced in both treated groups. Release was obtained by immunological challenge of AM from control patients after passive sensitization with atopic serum. The release of mediators with bronchoconstriction activity by AM could represent an alternative causal pathway in human asthma.

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