Molecular Microbiology Research Laboratory, Institute of Pharmaceutical Sciences, 150 Stamford Street, Franklin-Wilkins Building, King's College London, London, SE1 9NH, UK.
J Cyst Fibros. 2011 Sep;10(5):357-65. doi: 10.1016/j.jcf.2011.05.002. Epub 2011 Jun 12.
Cystic Fibrosis (CF) lung disease is characterised by an inexorable decline in lung function, punctuated by periods of symptomatic worsening known as pulmonary exacerbations (referred to here as CFPE). Despite their clinical significance, the cause of CFPE remains undetermined. It has been suggested that an increase in bacterial density may be a trigger, although this has not been shown empirically.
Here, a previously validated quantitative PCR-based approach was used to assess numbers of Pseudomonas aeruginosa and of total bacteria in respiratory secretions from patients during the period leading up to CFPE. Sputum samples collected from 12 adult CF patients were selected retrospectively to fall approximately 21, 14, 7 and 0 days prior to CFPE diagnosis. In addition, the relationships between clinical parameters (FEV(1), temperature and patient reported outcome measures) and microbiological data were investigated.
No significant changes either in total bacterial or P. aeruginosa numbers were identified prior to CFPE. Of all the correlations tested, only temperature showed a significant correlation with total bacterial numbers in the period leading to CFPE.
These findings strongly suggest that CFPE do not generally result from increased bacterial density within the airways. Instead, data presented here are consistent with alternative models of pulmonary exacerbation.
囊性纤维化(CF)肺部疾病的特征是肺功能不可避免地下降,期间会出现症状恶化的时期,称为肺部恶化(这里称为 CFPE)。尽管它们具有临床意义,但 CFPE 的原因仍未确定。有人认为细菌密度的增加可能是一个诱因,但这尚未得到经验证据的支持。
在这里,使用了先前经过验证的基于定量 PCR 的方法来评估 CFPE 前一段时间内呼吸道分泌物中铜绿假单胞菌和总细菌的数量。回顾性选择了来自 12 名成年 CF 患者的痰液样本,大约在 CFPE 诊断前 21、14、7 和 0 天采集。此外,还研究了临床参数(FEV1、体温和患者报告的结果测量)与微生物学数据之间的关系。
在 CFPE 之前,总细菌或铜绿假单胞菌数量均未发生明显变化。在所有测试的相关性中,只有体温在 CFPE 前的一段时间内与总细菌数量呈显著相关性。
这些发现强烈表明 CFPE 通常不是由于气道内细菌密度增加引起的。相反,这里提供的数据与肺部恶化的替代模型一致。