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Asthma and COPD are characterised by persistent airway inflammation and airway fibrosis. We have hypothesised that the inflammation is due to persistent immune stimulation by exogenous cigarette smoke in COPD and by activated airway resident cells, such as fibroblasts, in asthma. The numbers of fibroblasts in the airway wall in patients with asthma and COPD has not been reported and there are currently no specific markers for fibroblasts available for use in formalin fixed tissue. Aim: To compare numbers of fibroblasts in FA and COPD and in smoking (SC) and nonsmoking controls (NC) without airflow obstruction. Methods: Transversesections of large airways were obtained at autopsy (FA, NC), at surgical resection (SC - FEV1>80%, mild COPD - FEV1<80%) and at transplantation (severe COPD - FEV1<20%). Sections were stained with HAM56 (Dako -alveolar and tissue macrophages). Cells with a long spindle shaped nucleus and cytoplasm, not staining positively for HAM56 (tissue resident macrophages) were defined as fibroblasts. Positively stained cells were counted in the submucosa (away from the smooth muscle) and were expressed per mm of the basement membrane. Results: NC SC FA COPD COPD (mild) (severe) Fibroblasts 2.4±2.5* 6.4±3.3** T4.2±7.8 7.1±3.2# 11.5±4.5 p<0.05NC v FA&COPD (severe), **SC v FA, # COPD (mild) v FA Conclusions: In FA, submucosal fibroblasts were increased in number compared with controls (smoking or not) and mild COPD. Only severe COPD differed from nonsmoking controls. Therefore, the number of fibroblasts may be related to the degree of airway inflammation and/or obstruction.


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