Schleimer R P, Fox C C, Naclerio R M, Plaut M, Creticos P S, Togias A G, Warner J A, Kagey-Sobotka A, Lichtenstein L M
J Allergy Clin Immunol. 1985 Aug;76(2 Pt 2):369-74. doi: 10.1016/0091-6749(85)90656-6.
The role of human basophils and mast cells in the pathogenesis of allergic diseases has been analyzed. Purified human basophils and mast cells release several known mediators of allergic reactions, including histamine, sulfidopeptide leukotrienes, kinin-forming enzymes, and, in the case of the mast cell, PGD2. These same mediators are released in vivo after experimental challenge in the upper airways with either allergen or cold, dry air, a stimulus used to simulate exercise-induced bronchospasm. The appearance of mast cell mediators in vivo after such challenges further implicates mast cells in the pathogenesis of allergic diseases of the airways that occur as a result of exposure to allergen or physical stimuli. During the LPR after experimental challenge of the upper airways, the pattern of mediators released (i.e., histamine, leukotrienes, and others, but no PGD2) suggests that basophils may contribute to the LPR. Antiallergic drugs that prevent mediator release in vitro, such as antihistamines, also prevent the appearance of mediators in vivo, strengthening both the validity of the in vitro test as a model of the disease and the hypothesis that mediator release is an essential element of the disease process. A model discussing the pathogenetic mechanism is presented.
人类嗜碱性粒细胞和肥大细胞在过敏性疾病发病机制中的作用已得到分析。纯化的人类嗜碱性粒细胞和肥大细胞会释放几种已知的过敏反应介质，包括组胺、硫肽白三烯、激肽形成酶，对于肥大细胞而言，还会释放前列腺素D2。在对上呼吸道进行实验性激发后，无论是使用变应原还是冷的干燥空气（一种用于模拟运动诱发支气管痉挛的刺激物），这些相同的介质都会在体内释放。在这种激发后，肥大细胞介质在体内的出现进一步表明肥大细胞参与了因接触变应原或物理刺激而发生的气道过敏性疾病的发病机制。在上呼吸道实验性激发后的迟发相反应期间，释放的介质模式（即组胺、白三烯等，但无前列腺素D2）表明嗜碱性粒细胞可能促成迟发相反应。在体外可阻止介质释放的抗过敏药物，如抗组胺药，也能阻止介质在体内出现，这既强化了体外试验作为疾病模型的有效性，也强化了介质释放是疾病过程关键要素的假说。本文提出了一个讨论发病机制的模型。
