title: Evidence of mast-cell activation in a subset of patients with eosinophilic chronic obstructive pulmonary disease.
abstract: Although asthma has been viewed mainly as an eosinophilic disease, and chronic obstructive pulmonary disease (COPD) as a neutrophilic disease, recent studies have shown increased neutrophil counts in severe asthma and sputum eosinophilia in some COPD patients. In an attempt to further characterise these two syndromes according to pathology, the current authors have conducted a study of induced sputum in 15 subjects with COPD, 17 asthmatics, and 17 nonatopic healthy individuals. Sputum was analysed for cytology and levels of eosinophil cationic protein (ECP), albumin, tryptase and soluble intercellular adhesion molecule-1. The COPD subjects differed from the asthmatics as they had higher sputum neutrophil and lower columnar epithelial cell counts, but there were no differences in any soluble marker studied. When compared to control subjects, both the asthmatic and COPD subjects had raised eosinophil counts and ECP levels. In a subset of COPD subjects with sputum eosinophilia (>3% of total cells), significantly increased levels of tryptase were detected. In conclusion, although chronic obstructive pulmonary disease is a more neutrophilic disease than asthma, the two diseases are difficult to distinguish on the basis of sputum levels of the soluble markers traditionally associated with asthma. However, a subset of patients with chronic obstructive pulmonary disease with airway eosinophilia and mast-cell activation might represent a distinct pathological phenotype.
authors.affiliation: Dept of Pneumology, Centre Hospitalier Universitaire Sart-Timan, University of Liege, Belgium. R.Louis@chu.ulg.ac.be
authors.forename: R E
authors.initials: RE
authors.lastname: Louis
authors.forename: D
authors.initials: D
authors.lastname: Cataldo
authors.forename: M G
authors.initials: MG
authors.lastname: Buckley
authors.forename: J
authors.initials: J
authors.lastname: Sele
authors.forename: M
authors.initials: M
authors.lastname: Henket
authors.forename: L C
authors.initials: LC
authors.lastname: Lau
authors.forename: P
authors.initials: P
authors.lastname: Bartsch
authors.forename: A F
authors.initials: AF
authors.lastname: Walls
authors.forename: R
authors.initials: R
authors.lastname: Djukanovic
mesh_terms: D000328:Adult; D000368:Aged; D000418:Albumins / Q000032:analysis; D001249:Asthma / Q000276:immunology* / Q000473:pathology*; D001798:Blood Proteins / Q000032:analysis; D047091:Eosinophil Granule Proteins; D004802:Eosinophilia / Q000276:immunology* / Q000473:pathology*; D005260:Female; D006801:Humans; D018836:Inflammation Mediators / Q000032:analysis; D018799:Intercellular Adhesion Molecule-1 / Q000032:analysis; D008297:Male; D008407:Mast Cells / Q000276:immunology* / Q000473:pathology*; D008875:Middle Aged; D029424:Pulmonary Disease, Chronic Obstructive / Q000276:immunology* / Q000473:pathology*; D012129:Respiratory Function Tests; D012260:Ribonucleases; D012697:Serine Endopeptidases / Q000032:analysis; D013183:Sputum / Q000737:chemistry*; D053802:Tryptases
chemical_list: D000418:Albumins; D001798:Blood Proteins; D047091:Eosinophil Granule Proteins; D018836:Inflammation Mediators; D018799:Intercellular Adhesion Molecule-1; D012260:Ribonucleases; D012697:Serine Endopeptidases; D053802:Tryptases