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Published online before print August 6, 2008, 10.1183/09031936.00145307
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Eur Respir J 2009; 33:61-67
Copyright ©ERS Journals Ltd 2009

Decreased FOXP3 expression in small airways of smokers with COPD

S. Isajevs1, I. Taivans1, G. Strazda1, U. Kopeika2, M. Bukovskis3, V. Gordjusina1 and A. Kratovska1

1 Dept of Pathology, Faculty of Medicine, University of Latvia, 2 Centre of Thoracic Surgery, and 3 Department of Pulmonology and Allergology, Pauls Stradins Clinical University Hospital, Riga, Latvia.

CORRESPONDENCE: S. Isajevs, Faculty of Medicine, University of Latvia, 1a Sarlotes street, LV-1001, Riga, Latvia, Fax: 371 7580569. E-mail: sergisajevs{at}inbox.lv

Keywords: Chronic obstructive pulmonary disease, FOXP3 T-regulatory cells, inflammation

Received: November 2, 2007
Accepted July 23, 2008

CD4+CD25+ FOXP3-positive T-regulatory cells have an important role in controlling immune and inflammatory reactions. The present authors hypothesise that these cells may be involved in the pathogenesis of chronic obstructive pulmonary disease (COPD). The aim of the present study was to characterise the expression of FOXP3 in large and small airways of nonsmokers, smokers with normal lung function and COPD patients.

A total of 19 nonsmokers, 20 smokers with normal lung function and 20 smokers with moderate COPD, undergoing lung resection for a solitary peripheral nonsmall cell carcinoma, were enrolled in the study. Immunohistochemical methods were used to evaluate FOXP3 expression in large and small airways.

Smokers with normal lung function and COPD patients had increased numbers of FOXP3-positive cells in large airways compared with nonsmokers. A positive correlation was observed between FOXP3 expression in large airways and smoked pack-yrs. In small airways, COPD patients had decreased numbers of FOXP3-positive cells, compared with asymptomatic smokers and nonsmokers, that negatively correlated with airflow obstruction.

To conclude, chronic obstructive pulmonary disease is characterised by upregulation of FOXP3-positive cells in large airways but a downregulation in small airways that correlated with airflow limitation. The results of the present study contribute to a better understanding of the pathogenesis of chronic obstructive pulmonary disease.




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Eur Respir JHome page
S. Isajevs, I. Taivans, G. Strazda, U. Kopeika, M. Bukovskis, V. Gordjusina, and A. Kratovska
From the authors:
Eur. Respir. J., July 1, 2009; 34(1): 285 - 286.
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