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Clinical Investigations: COPD |

Relationships Among Bacteria, Upper Airway, Lower Airway, and Systemic Inflammation in COPD*

John R. Hurst, MB, ChB; Tom M. A. Wilkinson, MB, BS; Wayomi R. Perera, MB, BS; Gavin C. Donaldson, PhD; Jadwiga A. Wedzicha, MD
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*From the Academic Unit of Respiratory Medicine, St. Bartholomew’s Hospital, London, UK.

Correspondence to: Jadwiga A. Wedzicha, MD, Academic Unit of Respiratory Medicine, Dominion House, St. Bartholomew’s Hospital, London, EC1A 7BE, UK; e-mail: J.A.Wedzicha@qmul.ac.uk



Chest. 2005;127(4):1219-1226. doi:10.1378/chest.127.4.1219
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Study objective: The upper and lower airways are continuous. While upper airway symptoms are common in COPD patients, with accumulating evidence to suggest increased nasal inflammation, the relationships among upper airway, lower airway, and systemic inflammatory indexes have not been studied. We aimed to confirm that there is heightened nasal inflammation in COPD patients, to test the hypothesis that the degree of upper airway inflammation relates to the degree of lower airway inflammation, and to investigate the underlying associations with bacterial carriage and the systemic inflammatory response.

Design: Prospective cohort study.

Setting: Outpatient Department, London Chest Hospital, London, UK.

Participants: Forty-seven patients with COPD and 12 control subjects of similar age, sex, and smoking status.

Measurements: Serum, nasal wash fluid, and sputum samples were obtained from 47 stable patients with COPD for the analysis of inflammatory indexes and bacterial colonization. Nasal wash fluid specimens were obtained from 12 control subjects.

Results: COPD patients had an increased nasal interleukin (IL)-8 concentration compared to control subjects (difference, 97.2 pg/mL; p = 0.009). The nasal IL-8 concentration in COPD patients correlated with that in sputum (r = 0.30; p = 0.039). In both the upper and lower airways of patients with COPD, the IL-8 concentration was associated with indexes of bacterial colonization. Patients colonized with a sputum potentially pathogenic microorganism had a higher total nasal bacterial load (difference, 1.5 log cfu/mL; p = 0.016). We did not find significant relationships between the degree of upper or lower airway inflammation, or bacterial carriage, and the systemic inflammatory response.

Conclusions: COPD is associated with an increased nasal concentration of the neutrophil chemoattractant protein IL-8, the degree of which reflects that present in the lower airway. A relationship between lower airway bacterial colonization, postnasal drip, and higher nasal bacterial load may suggest a mechanism underlying this finding. This study is the first to report a correlation between the degree of upper and lower airway inflammation in COPD.

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