title: Chronic obstructive pulmonary disease: role of bronchiolar mast cells and macrophages.
abstract: Chronic obstructive pulmonary disease (COPD) is considered to be caused in part by smoking-induced inflammation, but it is unknown which inflammatory cells within the small airways are associated with the obstruction. We investigated the inflammatory infiltrate in the small airways of 16 current or ex-smokers with COPD (FEV1 < or = 75% predicted) and 15 without COPD (FEV1 > or = 85% predicted) in pneumectomy specimens that were removed for lung cancer. Mast cells, macrophages, neutrophils, eosinophils, T cells, and B cells were identified using immunohistochemistry on formalin-fixed, paraffin-embedded specimens. These cells were quantified in the epithelium and the remainder of the airway wall. The number of mast cells and macrophages in the epithelium, but not in the remainder of the airway wall, was significantly increased in patients with COPD. Neutrophil and T cell numbers did not differ between the groups. Only few B cells and eosinophils were present in both groups. Smoking history, perioperative steroid usage, tumor localization, or reversibility in the FEV1 to salbutamol could not account for the observed differences. We conclude that the number of epithelial mast cells and macrophages is increased in the bronchioli in smokers with airflow limitation, suggesting a role in development of COPD.
authors.affiliation: Department of Pulmonology, Leiden University Medical Center, The Netherlands.
authors.forename: W F
authors.initials: WF
authors.lastname: Grashoff
authors.forename: J K
authors.initials: JK
authors.lastname: Sont
authors.forename: P J
authors.initials: PJ
authors.lastname: Sterk
authors.forename: P S
authors.initials: PS
authors.lastname: Hiemstra
authors.forename: W I
authors.initials: WI
authors.lastname: de Boer
authors.forename: J
authors.initials: J
authors.lastname: Stolk
authors.forename: J
authors.initials: J
authors.lastname: Han
authors.forename: J M
authors.initials: JM
authors.lastname: van Krieken
mesh_terms: D000328:Adult; D000368:Aged; D015703:Antigens, CD / Q000378:metabolism; D015214:Antigens, Differentiation, Myelomonocytic / Q000378:metabolism; D001980:Bronchi / Q000166:cytology; D002452:Cell Count; D053818:Chymases; D003430:Cross-Sectional Studies; D004804:Eosinophils / Q000502:physiology; D004847:Epithelial Cells; D005260:Female; D006801:Humans; D007124:Immunoenzyme Techniques; D018836:Inflammation Mediators / Q000378:metabolism; D008173:Lung Diseases, Obstructive / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*; D008214:Lymphocytes / Q000502:physiology; D008264:Macrophages / Q000502:physiology*; D008297:Male; D008407:Mast Cells / Q000502:physiology*; D008875:Middle Aged; D009504:Neutrophils / Q000502:physiology; D012129:Respiratory Function Tests; D012189:Retrospective Studies; D012697:Serine Endopeptidases / Q000378:metabolism; D012907:Smoking / Q000009:adverse effects; D053802:Tryptases; D000097382:CD68 Molecule
chemical_list: D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D053818:Chymases; D018836:Inflammation Mediators; D012697:Serine Endopeptidases; D053802:Tryptases; C067980:CD68 antigen, human; D000097382:CD68 Molecule; C083294:chymase 2