Nitrotyrosine immunostaining and cellular inflammation in COPD

F. L. M. Ricciardolo, A. Rossi, C. F. Donner, A. Di Stefano (Bergamo, Veruno, Italy)

Source: Annual Congress 2001 - Inflammatory mechanisms of COPD
Session: Inflammatory mechanisms of COPD
Session type: Oral Presentation
Number: 2114
Disease area: Airway diseases

Congress or journal article abstract

Abstract

Reactive nitrogen species (RNS) seem to be involved in COPD pathobiology. Recently, it has been shown a correlation between COPD severity and nitrotyrosine (NT), a marker of RNS production, in induced sputum. We hypothesized that NT should be overexpressed in bronchial biopsies of COPD patients with increased cellular inflammation. We studied NT expression and T-cell number in bronchial biopsies of control, 5 non-smokers (117.4±]4.6 FEV1 %pred) and 8 smokers (104.8±]4.4 FEV1 %pred), and COPD groups, 12 mild/moderate (69.5±]2.6 FEV1 %pred) and 8 severe (33.1±]4.2 FEV1 %pred). Cryostatic sections were immunostained for quantification (positive cells/mm2) of T-lymphocytes (CD3+, CD4+ and CD8+) and for semi-quantitative analysis (score:0-3) of NT intensity and distribution in the submucosa. CD3+ and CD8+ number was significantly higher in mild/moderate COPD (588±]58 cell/mm2 [p=0.02] and 300±]30 cell/mm2 [p=0.04], respectively) than in control non-smokers (340±]50 cell/mm2 and 182±]33 cell/mm2, respectively). NT intensity was increased in mild/moderate COPD (score:1.22±]0.3 [p=0.05]) compared to control non-smokers (score:0.7±]0.2). We also found a positive correlation between FEV1%pred and NT distribution in all COPD patients (Rho=0.44, p=0.05). We conclude that NT is upregulated in mild/moderate COPD in association with an increased T-cell infiltration, and that NT correlates positively with the degree of airway caliber in COPD. This study suggests a role for RNS in mild COPD.


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F. L. M. Ricciardolo, A. Rossi, C. F. Donner, A. Di Stefano (Bergamo, Veruno, Italy). Nitrotyrosine immunostaining and cellular inflammation in COPD. Eur Respir J 2001; 16: Suppl. 31, 2114

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