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Association of mast cells with lung function in chronic obstructive pulmonary disease.

Authors :
Gosman, Margot M. E.
Postma, Dirkje S.
Vonk, Judith M.
Rutgers, Bea
Lodewijk, Monique
Smith, Mieke
Luinge, Marjan A.
ten Hacken, Nick H. T.
Timens, Wim
Source :
Respiratory Research; 2008, Vol. 9, Special section p1-9, 9p, 1 Color Photograph, 2 Charts, 2 Graphs
Publication Year :
2008

Abstract

Background: In asthma, higher chymase positive mast cell (MC-C) numbers are associated with less airway obstruction. In COPD, the distribution of MC-C and tryptase positive mast cells (MC-T) in central and peripheral airways, and their relation with lung function, is unknown. We compared MC-T and MC-C distributions in COPD and controls without airflow limitation, and determined their relation with lung function. Methods: Lung tissue sections from 19 COPD patients (median [interquartile range] FEV<subscript>1</subscript>% predicted 56 [23-75]) and 10 controls were stained for tryptase and chymase. Numbers of MC-T and MC-C were determined in different regions of central and peripheral airways and percentage of degranulation was determined. Results: COPD patients had lower MC-T numbers in the subepithelial area of central airways than controls. In COPD, MC-T numbers in the airway wall and more specifically in the epithelium and subepithelial area of peripheral airways correlated positively with FEV<subscript>1</subscript>/VC (Spearman's rho (rs) 0.47, p = 0.05 and rs 0.48, p = 0.05, respectively); MC-C numbers in airway smooth muscle of peripheral airways correlated positively with FEV<subscript>1</subscript>% predicted (rs 0.57, p = 0.02). Both in COPD patients and controls the percentage of degranulated MC-T and MC-C mast cells was higher in peripheral than in central airways (all p < 0.05), but this was not different between the groups. Conclusion: More MC-T and MC-C in peripheral airways correlate with better lung function in COPD patients. It is yet to determine whether this reflects a protective association of mast cells with COPD pathogenesis, or that other explanations are to be considered. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
14659921
Volume :
9
Database :
Complementary Index
Journal :
Respiratory Research
Publication Type :
Academic Journal
Accession number :
35700274
Full Text :
https://doi.org/10.1186/1465-9921-9-64