Zhang Ding, Xia Jingwen, Chen Xiaodong
Department of Respiratory Disease, Huashan Hospital, Fudan University, Shanghai, China.
Arch Bronconeumol. 2010 Sep;46(9):459-65. doi: 10.1016/j.arbres.2010.04.010. Epub 2010 Jun 22.
Many asthma exacerbations are caused by respiratory viral infections that induce the interplay between Th1 and Th2 immune responses. However, the time trends for Th1 and Th2 immune responses during these phenomena have not been well studied.
To identify possible mechanisms underlying the link between respiratory viral infections and asthma exacerbations.
We recruited 40 adults aged 21-58 years for 4 groups. A. Healthy, B. Healthy with viral infection, C. Mild to moderate asthma and D. Same as C, but with viral infection. Th1 and Th2 cytokines in induced sputum samples during the course of acute upper respiratory viral infections in otherwise healthy and asthmatic individuals were monitored. IL-4, IL-5 and IFN-γ were assayed by ELISA. Viral infection symptoms and asthma severity scores were monitored. Time trends were analyzed using linear mixed models.
IL-4 and IL-5 levels in groups C and D were higher than in groups A and B. IFN-γ levels and viral infection symptoms scores in group B spiked by day 2 and rapidly declined by day 7, while in group D, IFN-γ and symptoms scores for viral infection and asthma peaked much later (days 3-5) and slowly declined. The ratios of IL-4 and IL-5 to IFN-γ in group D were significantly higher than in group C.
Infection-induced asthma exacerbations may be due to impaired anti-viral Th1-immune responses. There appears to be a critical window of 3-5 days for therapeutic intervention.
许多哮喘加重是由呼吸道病毒感染引起的,这些感染会引发Th1和Th2免疫反应之间的相互作用。然而,在这些现象中Th1和Th2免疫反应的时间趋势尚未得到充分研究。
确定呼吸道病毒感染与哮喘加重之间联系的潜在机制。
我们招募了40名年龄在21至58岁之间的成年人,分为4组。A.健康组,B.感染病毒的健康组,C.轻度至中度哮喘组,D.与C组相同,但感染病毒。监测了健康个体和哮喘个体在急性上呼吸道病毒感染过程中诱导痰样本中的Th1和Th2细胞因子。通过酶联免疫吸附测定法检测白细胞介素-4(IL-4)、白细胞介素-5(IL-5)和干扰素-γ(IFN-γ)。监测病毒感染症状和哮喘严重程度评分。使用线性混合模型分析时间趋势。
C组和D组中的IL-4和IL-5水平高于A组和B组。B组中的IFN-γ水平和病毒感染症状评分在第2天达到峰值,并在第7天迅速下降,而在D组中,病毒感染和哮喘的IFN-γ及症状评分在更晚的时候(第3至5天)达到峰值,并缓慢下降。D组中IL-4和IL-5与IFN-γ的比值显著高于C组。
感染诱发的哮喘加重可能是由于抗病毒Th1免疫反应受损。似乎存在一个3至5天的关键治疗干预窗口期。