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Decreased macrophage release of TGF-ß and TIMP-1 in chronic obstructive pulmonary disease

¹ Serveis de Analisis Clinics, ² Pneumologia, and ³ Unitat de Investigació, Hospital Universitari Son Dureta, IUNICS (Institut Universitari d'Investigació en Ciències de la Salut), Palma de Mallorca, Spain.

CORRESPONDENCE: J. Sauleda, Servei Pneumologia, Hospital Universitari, Son Dureta, Andrea Doria 55, 07014 Palma Mallorca, Spain. Fax: 34 971175228. E-mail: jsauleda@hsd.es

Keywords: Chronic obstructive pulmonary disease, leukotrienes, oxidative stress, tissue inhibitor of metalloproteinase-1, transforming growth factor-ß₁

Received: March 17, 2004
Accepted March 21, 2005

The present study tested the hypothesis that alveolar macrophages (AM) from patients with chronic obstructive pulmonary disease (COPD) release more pro-inflammatory and/or less anti-inflammatory mediators than those from smokers with normal lung function and never-smokers.

AM were sorted by flow cytometry from bronchoalveolar lavage fluid in 13 patients with COPD (mean±SEM 67±2 yrs, forced expiratory volume in one second (FEV₁) 61±4% reference), 16 smokers with normal lung function (55±2 yrs, FEV₁ 97±4% reference) and seven never-smokers (67±7 yrs, FEV₁ 94±4% reference). After sorting, AM were cultured (with and without lipopolysaccharide stimulation) after 4 h and 24 h, and the concentrations of leukotriene B₄ (LTB₄), transforming growth factor (TGF)-ß₁ and tissue inhibitor of metalloproteinase (TIMP)-1 were quantified in the supernatant by ELISA. The production of reactive oxygen intermediates (ROI) in freshly isolated AM was determined by flow cytometry.

LTB₄ secretion and ROI production were not different between groups. In contrast, AM from COPD patients released significantly less TGF-ß₁ and TIMP-1 than those from smokers with normal lung function and nonsmokers.

In conclusion, these observations are compatible with reduced anti-inflammatory and anti-elastolytic capacity in chronic obstructive pulmonary disease, which is likely to contribute to the pathogenesis of the disease.

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