BRONCHOALVEOLAR NEUTROPHILIA DURING LATE ASTHMATIC REACTIONS INDUCED BY TOLUENE DIISOCYANATE
BRONCHOALVEOLAR NEUTROPHILIA DURING LATE ASTHMATIC REACTIONS INDUCED BY TOLUENE DIISOCYANATE
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DOI：
10.1164/ajrccm/136.1.36
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发表时间：
1987-07-01
期刊：
影响因子：
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通讯作者：
MAPP, CE
中科院分区：
文献类型：
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作者：
FABBRI, LM;BOSCHETTO, P;MAPP, CE
甲苯二异氰酸酯 (TDI) 是一种低分子量化学物质，可导致暴露对象出现职业性哮喘，其诱发晚期哮喘反应的机制尚不清楚。我们研究了 TDI 引起的早期和晚期哮喘反应是否与气道对乙酰胆碱反应性的变化以及支气管肺泡灌洗确定的气道炎症有关。我们在接触 TDI 之前和之后定期测量 FEV1，并在 TDI 后 8 小时对 6 名出现晚期哮喘反应的受试者和 6 名仅出现早期哮喘反应的受试者进行乙酰甲胆碱和支气管肺泡灌洗的剂量反应曲线。 TDI 后 2 小时，对一组 6 名先前记录有晚期哮喘反应的受试者和一组 6 名受试者在 TDI 后没有任何先前记录的哮喘反应进行了相同的操作。在出现晚期哮喘反应的受试者中，中性粒细胞在 2 小时和 8 小时均增加，而嗜酸性粒细胞和气道反应性仅在 8 小时增加。相比之下，早期哮喘反应受试者的中性粒细胞、嗜酸性粒细胞和气道反应性在 TDI 后 8 小时或正常对照受试者中 TDI 后 2 小时没有增加。这些结果表明，TDI 的晚期哮喘反应以及相关的气道反应性增加可能是由气道炎症引起的。
The mechanism by which late asthmatic reactions are induced by toluene diisocyanate (TDI), a low molecular weight chemical that causes occupational asthma in exposed subjects, is unknown. We investigated whether early and late asthmatic reactions induced by TDI are associated with changes in airway responsiveness to methacholine and airway inflammation as determined by bronchoalveolar lavage. We measured FEV1 before and at regular intervals after exposure to TDI, and performed dose-response curves to methacholine and bronchoalveolar lavage at 8 h after TDI in a group of 6 subjects wtih late asthmatic reactions and in 6 subjects with only early asthmatic reactions. The same procedure was followed 2 h after TDI in a group of 6 subjects with previously documented late asthmatic reactions and in a group of 6 subjects without any previously documented asthmatic reaction after TDI. In subjects with late asthmatic reactions, neutrophils were increased, at both 2 and 8 h, and eosinophils and airway responsiveness were increased only at 8 h. By contrast, neutrophils, eosinophils and airway responsiveness were not increased at 8 h after TDI in subjects with an early asthmatic reaction or at 2 h after TDI in normal control subjects. These results suggest that late asthmatic reactions to TDI, and the associated increase in airway responsiveness, may be caused by airway inflammation.