论文部分内容阅读
目的 探讨支气管哮喘 (简称哮喘 )肺内嗜酸粒细胞 (Eos)增多与Eos凋亡的关系。方法 采用卵蛋白致敏的豚鼠哮喘模型 ,动态观察肺组织病理学、支气管肺泡灌洗液 (BALF)细胞学和Eos凋亡的变化。结果 致敏豚鼠抗原激发后 ,血管周围Eos迁移和浸润主要发生在 2 4h以内 ,而支气管周围Eos浸润和BALF内Eos增高持续 1周以上。哮喘豚鼠第 2 4,48,72hEos凋亡率分别为 (2 .1± 1.3 ) % ,(3 7± 2 3 ) % ,(4 6± 2 7) % ,显著低于正常豚鼠 [(10 .1±3 4) % ,P <0 .0 5 ] ,至 168h才接近于正常水平。糖皮质激素地塞米松治疗使Eos凋亡率显著增加 [(3 4 .1± 12 .2 ) % ,P<0 .0 1] ,伴随气道炎症消退。结论 哮喘Eos凋亡抑制可能是肺内Eos浸润增加的一个重要机制
Objective To investigate the relationship between the increase of intrapulmonary eosinophils (Eos) and the apoptosis of Eos in bronchial asthma (asthma). Methods The asthmatic model of guinea pig sensitized with ovalbumin was used to observe the change of lung histopathology, the cytology of bronchoalveolar lavage fluid (BALF) and the apoptosis of Eos. Results Eosinophil migration and infiltration in perivascular area mainly occurred within 24 hours after antigen challenge in guinea pigs, whereas Eos infiltration around bronchus and Eos increased in BALF for more than 1 week. The apoptotic rate of asthmatic guinea pigs in the 2nd, 4th, 48th and 72th hour were (2. 1 ± 1.3)%, (37 ± 23)%, (46 ± 27)%, 1 ± 3 4)%, P <0. 05], until 168h was close to the normal level. Glucocorticoid dexamethasone treatment significantly increased the apoptosis rate of Eos [(34.1 ± 12.2)%, P <0.01], accompanied by regression of airway inflammation. Conclusion Inhibition of Eos apoptosis in asthma may be an important mechanism of increased Eos infiltration in the lung