Wilkinson Tom M A, Hurst John R, Perera Wayomi R, Wilks Mark, Donaldson Gavin C, Wedzicha Jadwiga A
Academic Unit of Respiratory Medicine, St. Bartholomew's and the Royal London School of Medicine, St. Bartholomew's Hospital, London, UK.
Academic Unit of Respiratory Medicine, St. Bartholomew's and the Royal London School of Medicine, St. Bartholomew's Hospital, London, UK.
Chest. 2006 Feb;129(2):317-324. doi: 10.1378/chest.129.2.317.
The inflammatory responses and associated clinical severity of COPD exacerbations are greatly variable, and the determinants of these factors are poorly understood. We examined the hypothesis that bacteria and viruses may modulate this heterogeneity and that interactions between bacterial and viral infection may affect changes in airway bacterial load and the clinical features and inflammatory responses of exacerbations in patients with COPD.
Prospective cohort study.
Outpatient Department, London Chest Hospital, London, UK.
Thirty-nine patients with COPD.
We prospectively studied 56 COPD exacerbations, obtaining clinical data and paired sputum and serum samples at baseline and exacerbation. Qualitative and quantitative microbiology, polymerase chain reaction detection for rhinovirus, and estimation of cytokine levels by enzyme-linked immunosorbent assay were performed.
A total of 69.6% of exacerbations were associated with a bacterial pathogen, most commonly Haemophilus influenzae. Rhinovirus was identified in 19.6% of exacerbations. The rise in bacterial load at exacerbation correlated with the rise in sputum interleukin (IL)-8 (r = 0.37, p = 0.022) and fall in FEV1 (r = 0.35, p = 0.048). Exacerbations with both rhinovirus and H. influenzae had higher bacterial loads (10(8.56) cfu/mL vs 10(8.05)cfu/mL, p = 0.018) and serum IL-6 (13.75 pg/mL vs 6.29 pg/mL, p = 0.028) than exacerbations without both pathogens. In exacerbations with both cold symptoms (a marker of putative viral infection) and a bacterial pathogen, the FEV1 fall was greater (20.3% vs 3.6%, p = 0.026) and symptom count was higher (p = 0.019) than those with a bacterial pathogen alone.
The clinical severity and inflammatory responses in COPD exacerbations are modulated by the nature of the infecting organism: bacterial and viral pathogens interact to cause additional rises in inflammatory markers and greater exacerbation severity.
慢性阻塞性肺疾病（COPD）急性加重期的炎症反应及相关临床严重程度差异很大，而这些因素的决定因素尚不清楚。我们检验了以下假设：细菌和病毒可能调节这种异质性，并且细菌和病毒感染之间的相互作用可能影响COPD患者气道细菌载量的变化以及急性加重期的临床特征和炎症反应。
前瞻性队列研究。
英国伦敦胸科医院门诊部。
39例COPD患者。
我们前瞻性地研究了56次COPD急性加重期，在基线期和急性加重期获取临床数据以及配对的痰液和血清样本。进行了定性和定量微生物学检测、鼻病毒的聚合酶链反应检测以及通过酶联免疫吸附测定法估算细胞因子水平。
总共69.6%的急性加重期与细菌病原体相关，最常见的是流感嗜血杆菌。在19.6%的急性加重期中检测到鼻病毒。急性加重期细菌载量的增加与痰液白细胞介素（IL）-8的升高相关（r = 0.37，p = 0.022），与第一秒用力呼气容积（FEV1）的下降相关（r = 0.35，p = 0.048）。同时感染鼻病毒和流感嗜血杆菌的急性加重期比未感染这两种病原体的急性加重期具有更高的细菌载量（10⁸·⁵⁶cfu/mL对10⁸·⁰⁵cfu/mL，p = 0.018）和血清IL-6水平（13.75 pg/mL对6.29 pg/mL，p = 0.028）。在同时有感冒症状（假定病毒感染的标志物）和细菌病原体的急性加重期中，FEV1的下降幅度更大（20.3%对3.6%，p = 0.026），症状数量更多（p = 0.019），高于仅感染细菌病原体的急性加重期。
COPD急性加重期的临床严重程度和炎症反应受感染病原体性质的调节：细菌和病毒病原体相互作用导致炎症标志物进一步升高，加重期严重程度增加。
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