Flint K C, Leung K B, Hudspith B N, Pearce F L, Brostoff J, Johnson N M
Respiration. 1986;50 Suppl 2:31-41. doi: 10.1159/000195099.
Mast cells may be recovered from human subjects by bronchoalveolar lavage. Such bronchoalveolar mast cells will release histamine in response to IgE-dependent challenge in a reaction that is dose-, time- and energy-dependent. They possess functional characteristics distinct from dispersed human lung mast cells. The percentage of mast cells within the bronchoalveolar cell population is critically dependent upon the underlying pathology. Greater numbers of mast cells may be recovered from the bronchoalveolar compartment of extrinsic asthmatics than from controls. In addition, bronchoalveolar mast cells from asthmatic subjects show an increased releasability of histamine in response to anti-IgE. Antigen challenge also leads to the release of histamine in vitro, demonstrating the potential for the antigen-specific initiation of bronchoconstriction in these subjects. Spontaneous release of histamine from bronchoalveolar mast cells of asthmatic subjects was also greater than in controls (up to 46%), a feature which may be related to non-immunological mechanisms of bronchoconstriction. Such non-immunological mechanisms have been further investigated utilising mannitol as a model of hyperosmolar histamine release. Mannitol induced a dose-dependent release of histamine from bronchoalveolar mast cells of normal subjects, and this release was significantly inhibited by sodium cromoglycate. The leukotrienes are putative major mediators of human asthma. After challenge with anti-IgE in vitro, dose-dependent release of leukotriene C4 and prostaglandin D2 occurs from the bronchoalveolar cells of normal subjects. The release of PGD2 shows significant correlation with histamine release. Lying superficially, bronchoalveolar mast cells would be readily accessible to inhaled antigen. Mediator release from such cells may be relevant to the pathogenesis of asthma.
肥大细胞可通过支气管肺泡灌洗从人体受试者中获取。此类支气管肺泡肥大细胞会在IgE依赖性刺激下释放组胺，该反应具有剂量、时间和能量依赖性。它们具有与分散的人肺肥大细胞不同的功能特征。支气管肺泡细胞群体中肥大细胞的百分比严重依赖于潜在的病理状况。与对照组相比，从外源性哮喘患者的支气管肺泡腔中可回收更多数量的肥大细胞。此外，哮喘患者的支气管肺泡肥大细胞对抗IgE刺激显示出组胺释放能力增强。抗原刺激在体外也会导致组胺释放，表明这些受试者存在抗原特异性引发支气管收缩的可能性。哮喘患者支气管肺泡肥大细胞组胺的自发释放也高于对照组（高达46%），这一特征可能与支气管收缩的非免疫机制有关。利用甘露醇作为高渗组胺释放模型对这种非免疫机制进行了进一步研究。甘露醇可诱导正常受试者支气管肺泡肥大细胞组胺呈剂量依赖性释放，且这种释放可被色甘酸钠显著抑制。白三烯被认为是人类哮喘的主要介质。在体外抗IgE刺激后，正常受试者支气管肺泡细胞会发生白三烯C4和前列腺素D2的剂量依赖性释放。PGD2的释放与组胺释放显著相关。支气管肺泡肥大细胞位于浅表位置，吸入的抗原很容易接触到它们。此类细胞的介质释放可能与哮喘的发病机制有关。
