Godard P, Chaintreuil J, Damon M, Coupe M, Flandre O, Crastes de Paulet A, Michel F B
J Allergy Clin Immunol. 1982 Aug;70(2):88-93. doi: 10.1016/0091-6749(82)90234-2.
Alveolar macrophages (AM) were obtained by bronchoalveolar lavage (BAL) from seven healthy nonallergic, nonasthmatic donors, 15 patients with allergic bronchial asthma, and six patients with aspirin-sensitive asthma. AM were purified by adherence over 2 hr and cultured for an additional 24 hr. Functional assessment of viable cells was carried out for zymosan phagocytosis and for prostaglandin (PG) E2-PGF2 alpha and thromboxane (Tx) B2 release by resting and zymosan-stimulated AM. The eosinophil count in BAL fluid from allergic asthmatics was higher than that from control subjects (3.9% +/- 1.6% vs 0.4% +/- 0.3%, p less than 0.05) and still greater in BAL from patients with aspirin-sensitive asthma (21.7% +/- 9.0%, p less than 0.01). After the 24 hr of incubation, the AM viability was inversely correlated to the percentage of eosinophils in BAL fluid (r = -0.54, n = 21, p less than 0.02). Zymosan phagocytosis was significantly lower by viable cells from both allergic asthmatics and aspirin-sensitive patients as compared with cells from normal donors (p less than 0.05). Zymosan phagocytosis induced a twofold to threefold increase in the release of PGE2, PGF2 alpha, and TxB2 from AM of normal subjects (p less than 0.01) but only a onefold to twofold increase from AM of allergic asthmatic patients. The stimulated AM from aspirin-sensitive patients released smaller quantities of each product than AM from normal subjects or allergic asthmatic patients (p less than 0.05). We conclude that the viability and functional activity of AM are impaired in asthmatic patients and that these deficits correlate with the percent eosinophilia in the BAL; it is therefore suggested that they may be due to an interaction between eosinophils and AM in the bronchoalveolar lumen.
通过支气管肺泡灌洗（BAL）从7名健康的非过敏、非哮喘供体、15名过敏性支气管哮喘患者和6名阿司匹林敏感性哮喘患者中获取肺泡巨噬细胞（AM）。通过2小时以上的贴壁法纯化AM，并再培养24小时。对存活细胞进行功能评估，检测其对酵母聚糖的吞噬作用以及静息和酵母聚糖刺激的AM释放前列腺素（PG）E2 - PGF2α和血栓素（Tx）B2的情况。过敏性哮喘患者BAL液中的嗜酸性粒细胞计数高于对照组（3.9%±1.6%对0.4%±0.3%，p<0.05），在阿司匹林敏感性哮喘患者的BAL液中更高（21.7%±9.0%，p<0.01）。孵育24小时后，AM活力与BAL液中嗜酸性粒细胞百分比呈负相关（r = -0.54，n = 21，p<0.02）。与正常供体的细胞相比，过敏性哮喘患者和阿司匹林敏感性患者的存活细胞对酵母聚糖的吞噬作用明显降低（p<0.05）。酵母聚糖吞噬作用使正常受试者的AM释放PGE2、PGF2α和TxB2增加2至3倍（p<0.01），但过敏性哮喘患者的AM仅增加1至2倍。阿司匹林敏感性患者受刺激的AM释放的每种产物量均低于正常受试者或过敏性哮喘患者的AM（p<0.05）。我们得出结论，哮喘患者AM的活力和功能活性受损，且这些缺陷与BAL中的嗜酸性粒细胞增多百分比相关；因此提示它们可能是由于支气管肺泡腔内嗜酸性粒细胞与AM之间的相互作用所致。
