CELLULAR EVENTS IN THE BRONCHI IN MILD ASTHMA AND AFTER BRONCHIAL PROVOCATION
CELLULAR EVENTS IN THE BRONCHI IN MILD ASTHMA AND AFTER BRONCHIAL PROVOCATION
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DOI：
10.1164/ajrccm/139.3.806
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发表时间：
1989-03-01
期刊：
影响因子：
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通讯作者：
HOLGATE, ST
中科院分区：
文献类型：
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作者：
BEASLEY, R;ROCHE, WR;HOLGATE, ST
我们对过敏性哮喘患者的支气管活检和支气管灌洗液进行了详细的细胞和超微结构检查，以确定轻度过敏性哮喘炎症过程的性质和程度。8名特应性哮喘患者（平均PC 20组胺，0.90 mg/ml）和4名非哮喘对照组进行了纤维支气管镜检查。所有哮喘受试者在支气管镜检查前临床稳定2周，不需要治疗或单独吸入沙丁胺醇。进行单次50 ml支气管冲洗，然后进行隆突下支气管内活检。这些程序重复哮喘受试者18小时后，支气管激发过敏原或乙酰甲胆碱。随后，所有受试者均接受吸入组胺的支气管反应性试验。临床和生理数据未透露给解释标本的病理学家。哮喘受试者比非哮喘受试者有显著更多的上皮细胞脱落到灌洗液中（7.23对1.48 ×104/ml，p = 0.048）。灌洗液上皮细胞计数与支气管反应性之间存在统计学显著负相关（rho =-0.64，p = 0.03）。在哮喘受试者中，而不是在对照组中，有广泛的胶原沉积在上皮基底膜下，肥大细胞脱粒，嗜酸性粒细胞的粘膜浸润，表现出活化的形态学证据。嗜酸性粒细胞、单核细胞和血小板与血管内皮细胞接触，哮喘受试者中嗜酸性粒细胞和单核细胞迁移。发现这些变化与过敏原的支气管激发无关。我们的结论是过敏性哮喘伴随着广泛的气道炎症变化，即使在轻微的临床和亚临床疾病。
We have undertaken detailed cellular and ultrastructural examination of bronchial biopsies and bronchial lavage fluid from allergic asthmatic patients in order to determine the nature and degree of the inflammatory processes in mild allergic asthma. Eight atopic asthmatic patients (mean PC20 histamine, 0.90 mg/ml) and four nonasthamtic control subjects underwent fiberoptic bronchoscopy. All asthmatic subjects were clinically stable for 2 wk prior to bronchoscopy and required either no treatment or inhaled albuterol alone. A single 50-ml bronchial wash was undertaken, followed by endobronchial biopsy of subcarinae. These procedures were repeated in the asthematic subjects 18 h after bronchial provocation with allergen or methacholine. Subsequently, all subjects underwent bronchial reactivity testing with inhaled histamine. The clinical and physiologic data were not revealed to the pathologist interpreting the specimens. The asthmatic subjects shed a significantly greater number of epithelial cells into the lavage fluid than did the nonasthmatic subjects (7.23 versus 1.48 .times. 104/ml, p = 0.048). There was a statistically significant inverse correlation between the lavage epithelial cell count and bronchial reactivity (rho = -0.64, p = 0.03). In the asthmatic subjects, but not in the control subjects, there was extensive deposition of collagen beneath the epithelial basement membrane, mast cell degranulation, and mucosal infiltration by eosinophils, which exhibited morphologic evidence of activation. Eosinophils, monocytes, and platelets were found in contact with the vascular endothelium, with emigration of eosinophils and monocytes in the asthamtic subjects. These changes were found irrespective of bronchial challenge with allergen. We conclude that allergic asthma is accompanied by extensive inflammatory changes in the airway, even in mild clinical and subclinical disease.