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Ongoing Airway Inflammation in Patients With COPD Who Do Not Currently Smoke*

Steven R. Rutgers, MD; Dirkje S. Postma, MD; Nick H. ten Hacken, MD; Henk F. Kauffman, PhD; Thomas W. van der Mark, PhD; Gerard H. Koëter, MD; Wim Timens, MD
Author and Funding Information

*From the Departments of Pulmonology (Drs. Rutgers, Postma, ten Hacken, van der Mark, and Koëter), Allergology (Dr. Kauffman), and Pathology (Dr. Timens), University Hospital Groningen, The Netherlands.

Correspondence to: W. Timens, MD, Professor of Pathology, University Hospital Groningen, PO Box 30.001, NL-9700 RB Groningen, Netherlands



Chest. 2000;117(5_suppl_1):262S. doi:10.1378/chest.117.5_suppl_1.262S
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Extract

Abbreviation: ECP = eosinophil cationic protein

Inflammation in the airways in COPD is largely attributed to smoking, yet this may be present even in ex-smokers. We studied changes in inflammatory cells and factors contributing to these changes in the airways of patients with COPD who do not currently smoke. We studied 18 nonatopic subjects with COPD (14 men and 4 women; mean ± SD age, 62 ± 8 years; FEV1, 59 ± 13% predicted) and 11 nonatopic healthy subjects (8 men and 3 women; age, 58 ± 8 years; FEV1, 104 ± 11% predicted). Sputum induction and bronchoscopy with BAL and biopsies were performed. Subjects with COPD had more mucosal CD68+ cells (median, 1,115 vs 590 cells/mm, p = 0.03) and EG2+ cells (40 vs. 5 cells/mm, p = 0.049) and a tendency towards more CD4+ but not CD8+ cells than healthy control subjects. Furthermore, subjects with COPD had higher percentages of sputum neutrophils (77% vs 36%, p = 0.001) and eosinophils (1.2% vs 0.2%, p = 0.008) and BAL fluid eosinophils (0.4% vs 0.2%, p = 0.03) and higher concentrations of sputum, eosinophil cationic protein (ECP) (838 vs 121 ng/mL, p < 0.001). Concentrations of ECP per eosinophil were not higher. Patients with COPD and high mucosal EG2+ cell numbers had high mucosal CD4+ cell numbers. Sputum eosinophilia was associated with a decrease in FEV1/vital capacity and BAL fluid eosinophilia with a decrease in mucosal NP57+ cells. We conclude that subjects with COPD who do not currently smoke have increased numbers of inflammatory cells. Eosinophils are increased in number in the airways in COPD but do not seem to be activated. The increased eosinophil numbers are probably due to recruitment as a result of ongoing inflammation. Macrophages and lymphocytes may play a role in this inflammation.

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