Wood Lisa G, Powell Heather, Grissell Terry, Nguyen Thuy T D, Shafren Darren, Hensley Michael, Gibson Peter G
School of Medicine and Public Health, University of Newcastle, Newcastle, NSW, Australia.
Chest. 2007 Feb;131(2):415-23. doi: 10.1378/chest.06-1062.
This study examined the contribution of airway inflammation to the delayed lung function recovery that occurs in some people following virus-induced asthma exacerbations.
Subjects (n = 40) were recruited at hospital admission for acute asthma exacerbation. Respiratory virus infection was diagnosed by viral nucleic acid detection and/or cell culture, using induced sputum, nasal, or throat swabs. Data collected included lung function, answers to common cold and asthma control questionnaires, and induced sputum cellular profiles. Subjects were reexamined 4 to 6 weeks postexacerbation and were compared with stable asthmatic subjects (n = 26) who had been recruited from ambulatory care clinics.
Persistent airway obstruction, defined as lung function improvement at follow-up (ie, change in FEV1 percent predicted [Delta%FEV1]) of <15%, was observed in 10 subjects (25%). Airway recovery (Delta%FEV1, > or = 15%) was observed in the remaining subjects (30 subjects; 75%). During the acute episode, the airway-recovery group had increased total cell count (p = 0.019), increased number of neutrophils (p = 0.005), and increased percentage of neutrophils (p = 0.0043) compared to the group of stable subjects with asthma. Postexacerbation, the airway-recovery group had reduced numbers of neutrophils and an increased percentage of eosinophils. In contrast, during exacerbation, subjects with persistent airway obstruction showed no differences in inflammatory cell counts compared to stable subjects with asthma, nor did cell counts change postexacerbation. Symptoms improved in both groups postexacerbation. However, in the persistent-airway-obstruction group, asthma remained uncontrolled.
Persistent airway obstruction and uncontrolled asthma are observed in some people after viral asthma exacerbations. These abnormalities are not associated with inflammatory cell influx into the airway lining fluid during the exacerbation and may reflect the involvement of noncellular elements. Further work should explore other mechanisms leading to incomplete airway recovery.
本研究探讨了气道炎症对某些人在病毒诱发哮喘加重后肺功能延迟恢复的影响。
招募因急性哮喘加重入院的受试者（n = 40）。通过病毒核酸检测和/或细胞培养，使用诱导痰、鼻拭子或咽拭子诊断呼吸道病毒感染。收集的数据包括肺功能、普通感冒和哮喘控制问卷的答案以及诱导痰细胞图谱。在加重后4至6周对受试者进行复查，并与从门诊诊所招募的稳定哮喘受试者（n = 26）进行比较。
10名受试者（25%）出现持续性气道阻塞，定义为随访时肺功能改善（即预测的第一秒用力呼气容积百分比变化[Δ%FEV1]）<15%。其余受试者（30名；75%）出现气道恢复（Δ%FEV1≥15%）。在急性发作期间，与稳定哮喘受试者组相比，气道恢复组的总细胞计数增加（p = 0.019）、中性粒细胞数量增加（p = 0.005）以及中性粒细胞百分比增加（p = 0.0043）。加重后，气道恢复组的中性粒细胞数量减少，嗜酸性粒细胞百分比增加。相比之下，在加重期间，持续性气道阻塞的受试者与稳定哮喘受试者相比，炎症细胞计数无差异，加重后细胞计数也未改变。两组加重后症状均有改善。然而，在持续性气道阻塞组中，哮喘仍未得到控制。
在病毒诱发哮喘加重后，一些人会出现持续性气道阻塞和未控制的哮喘。这些异常与加重期间炎症细胞流入气道衬液无关，可能反映了非细胞成分的参与。进一步的研究应探索导致气道恢复不完全的其他机制。
