Terpstra G K, Kreukniet J, Raaijmakers J A
Eur J Respir Dis Suppl. 1984;135:34-46.
The B. pertussis model of atopy as proposed by Szentivanyi in 1968 has been a starting point for much research involving the pathogenesis of COLD. Moreover, it supplied more insight into the pharmaco-therapeutic approach toward this group of diseases. In this review, it is shown that products of bacteria considered to be a constituent of the normal flora of the human upper respiratory tract, such as H. influenzae, elicit changes in adrenoceptor responsiveness which are compatible with an enhanced tendency toward bronchoconstriction. One of the features of human atopy is enhanced mediator release after appropriate stimuli resulting in bronchoconstriction. This phenomenon can be mimicked in an animal model, the H. influenzae-vaccinated rat or guinea pig; enhanced histamine synthesis and release are found in vivo as well as in vitro. The effects point in the direction of a beta-adrenergic defect which is not only demonstrable in biochemical but also in physiologically oriented parameters. Pulmonary smooth muscle tissue appears to be less responsive to beta-adrenergic agonists and has an enhanced tendency to contract. The view that these changes are indeed the reflection of changes in adrenoceptor systems has been investigated in guinea pigs and rats. In both species impairment of beta-adrenergic systems together with a reduction in the number of beta 2-adrenoceptors was found after vaccination. Also the involvement of other factors, e.g., catecholamines, has been demonstrated. Comparable changes occur within the pulmonary adrenoceptor populations of COLD patients, suggesting disturbed homeostasis in the autonomic nervous system, possibly leading to bronchoconstriction. The question whether a bacterial factor is important in these changes and might induce, sustain or enhance the effects of other factors or even have a role in the pathogenesis of COLD is discussed in this review.
1968年由森蒂瓦尼提出的百日咳杆菌特应性模型一直是许多涉及感冒发病机制研究的起点。此外，它为针对这类疾病的药物治疗方法提供了更多见解。在这篇综述中，研究表明，被认为是人类上呼吸道正常菌群组成部分的细菌产物，如流感嗜血杆菌，会引发肾上腺素能受体反应性的变化，这与支气管收缩倾向增强相一致。人类特应性的特征之一是在适当刺激后介质释放增加，导致支气管收缩。这种现象可以在动物模型中模拟，即接种流感嗜血杆菌的大鼠或豚鼠；在体内和体外都发现组胺合成和释放增加。这些效应指向β-肾上腺素能缺陷的方向，这不仅在生化参数中可以证明，在生理学参数中也可以证明。肺平滑肌组织对β-肾上腺素能激动剂的反应似乎较弱，并且有增强的收缩倾向。在豚鼠和大鼠中研究了这些变化确实是肾上腺素能受体系统变化反映的观点。在这两个物种中，接种疫苗后均发现β-肾上腺素能系统受损以及β2-肾上腺素能受体数量减少。还证明了其他因素的参与，例如儿茶酚胺。在感冒患者的肺肾上腺素能受体群体中也发生了类似的变化，这表明自主神经系统的稳态受到干扰，可能导致支气管收缩。本文综述讨论了细菌因素在这些变化中是否重要，是否可能诱导、维持或增强其他因素的作用，甚至在感冒发病机制中是否起作用的问题。
