Small airway inflammation in chronic obstructive pulmonary disease (COPD)
W. M. Elliott, D. Ionescu, B. Meshi, S. Utokaparch, R. M. Rogers, F. C. Sciurba, P. D. Pare, J. C. Hogg (Vancouver, Canada; Pittsburgh, United States Of America)
Source: Annual Congress 2001 - Inflammation and genetics in airway disease
Session: Inflammation and genetics in airway disease
Session type: Oral Presentation
Number: 3382
Disease area: Airway diseases
Abstract Background: Cigarette smoking causes airway inflammation in everyone but only a proportion of smokers develop COPD.Purpose: To test the hypothesis that airway obstruction is caused by an amplification of the cigarette smoke induced inflammatory response.Methods: Lung tissue was obtained from heavy smokers with nomal lung function (n=7), mild (n=7) or severe COPD (n=7). Quantitative analysis was performed based on a cascade design using CT lung volume as a reference volume and histologic point counting to establish the volume fraction Vv of small airways, inflammatory cells total collagen and subtypes.Results: Inflammatory cells/ml airway tissue increased in severe COPD (p = 0.02) due to increased numbers of macrophages, CD-8, and B-lymphocytes. The PMN increased in the epithelium whereas the CD-8, CD-4, B-lymphocytes and macrophages increased in the adventitia and were associated with increased lymphoid follicle formation. Eosinophils were low in number and unchanged with disease. Total collagen did not change but shifted in type and associated with a reduced airway lumen in severe COPD.Conclusion: The small airway inflammatory response is amplified, and associated with a proliferation of lymphoid follicles, rearrangement of collagen and a reduced airway lumen in smokers that develop severe COPD.
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W. M. Elliott, D. Ionescu, B. Meshi, S. Utokaparch, R. M. Rogers, F. C. Sciurba, P. D. Pare, J. C. Hogg (Vancouver, Canada; Pittsburgh, United States Of America). Small airway inflammation in chronic obstructive pulmonary disease (COPD). Eur Respir J 2001; 16: Suppl. 31, 3382
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