文摘

哮喘气道炎症,可现在,诱导痰的分析评估。10例哮喘患者调查期间急性恶化的量化细胞凋亡,bcl - 2和Fas表达,诱导痰淋巴细胞。他们相比12慢性阻塞性肺疾病(COPD)患者和10个健康对照。自发凋亡是由与propidium碘染色细胞核,FACScan和分析。bcl - 2被西方墨点法测量,并通过光密度扫描结果,由凝胶proanalyser完成。Fas的调查进行了使用streptavidin-biotin preroxidase-complex方法。患者哮喘和COPD患者表现出细胞结构的显著增加,中性粒细胞、嗜酸性粒细胞和淋巴细胞的比例与健康对照组相比。细胞凋亡诱导痰里发现单核细胞减少哮喘患者相比,慢性阻塞性肺病患者和健康对照组。细胞凋亡的定量测量在暴露于anticytokine抗体。Anti-TNF-α抗体阻止了细胞凋亡在患者组和健康对照组,表明TNF-α作为细胞凋亡的诱导物。 Anti-IL-10 blocked apoptosis completely exclusively in patients with asthma. Bcl-2 expression was found to be increased in induced sputum mononuclear cells from patients with asthma, compared to healthy controls and patients with COPD. Expression of Fas could be detected in patients with asthma, at a lower level than COPD patients and healthy controls. Distinct mechanisms of apoptosis were found in patients with asthma and patients with COPD, characterized by different levels of Bcl-2 and Fas expression. Induction of apoptosis should be a beneficial process in allergic inflammation traduced in induced sputum mononuclear cells. The apoptosis process is assumed by two different mechanisms in asthma and COPD. Our findings indicated that in asthmatic patients, activated lymphocytes accumulate in the bronchi; because of their prolonged survival that maintains inflammation.