IMMEDIATE AND LATE AIRWAY RESPONSE OF ALLERGIC RHINITIS PATIENTS TO SEGMENTAL ANTIGEN CHALLENGE - CHARACTERIZATION OF EOSINOPHIL AND MAST-CELL MEDIATORS
IMMEDIATE AND LATE AIRWAY RESPONSE OF ALLERGIC RHINITIS PATIENTS TO SEGMENTAL ANTIGEN CHALLENGE - CHARACTERIZATION OF EOSINOPHIL AND MAST-CELL MEDIATORS
复制标题
DOI：
10.1164/ajrccm/144.6.1274
复制
发表时间：
1991-12-01
期刊：
影响因子：
--
通讯作者：
BUSSE, WW
中科院分区：
文献类型：
--
作者：
SEDGWICK, JB;CALHOUN, WJ;BUSSE, WW
节段性抗原支气管激发用于确定过敏性呼吸道疾病炎症过程的性质。变应性鼻炎患者节段性抗原滴注后12min的支气管肺泡灌洗液(即刻反应)显示组胺和类胰蛋白酶显著升高，但无细胞反应。重复节段性灌洗48h后(延迟反应)，低密度和正常密度的嗜酸性粒细胞均显著增加，嗜酸性粒细胞颗粒蛋白(主要碱性蛋白、嗜酸性粒细胞衍生的神经毒素、嗜酸性粒细胞阳离子蛋白和嗜酸性粒细胞过氧化物酶)水平显著升高。白三烯C4，但不是类胰蛋白酶，在后期灌洗样本中浓度也持续升高。此外，后期洗液样本显示白细胞介素5浓度显著增加，这与嗜酸性粒细胞和嗜酸性粒细胞颗粒蛋白的存在有关。当正常受试者接受类似的抗原攻击时，嗜酸性粒细胞和嗜酸性粒细胞的可溶性介体都不会增加。这些数据表明，在变态反应后期，嗜酸性粒细胞被吸引到呼吸道，IL-5可能会引起气道嗜酸性粒细胞密度的变化，并促进颗粒蛋白的释放，从而导致气道损伤。
Segmental antigen bronchoprovocation was used to define the nature of the inflammatory process in allergic airway disease. Bronchoalveolar lavage fluid obtained from allergic rhinitis patients 12 min after segmental antigen instillation (immediate response) revealed a significant increase in histamine and tryptase, but no cellular response. Repeat segmental lavage 48 h later (late response) showed marked and significant increases in both low and normal density eosinophils as well as striking elevations of eosinophil granular protein levels (major basic protein, eosinophil-derived neurotoxin, eosinophil cationic protein, and eosinophil peroxidase). Leukotriene C4, but not tryptase, concentrations were also consistently elevated in late lavage samples. Further, the late lavage samples showed a significant increase in interleukin-5 concentrations that correlated with the presence of eosinophils and eosinophil granular proteins. Neither eosinophils nor soluble mediators of eosinophils increased when normal subjects were similarly challenged with antigen. These data suggest that eosinophils are attracted to the airway during the late-phase allergic reaction and that IL-5 may produce changes in airway eosinophil density and promote the release of granular proteins to cause airway injury.