Induced sputum CD8 + T-lymphocyte subpopulations in chronic obstructive pulmonary disease

• Published in: Respiratory medicine Vol. 98; no. 1; pp. 57 - 65
• Main Authors: Tzanakis, Nikolaos, Chrysofakis, Georgios, Tsoumakidou, Maria, Kyriakou, Despina, Tsiligianni, Joanna, Bouros, Demosthenes, Siafakas, Nikolaos M
• Format: Journal Article
• Language: English
• Published: Oxford Elsevier Ltd 2004; Elsevier; Elsevier Limited
• Subjects: Aged; Biological and medical sciences; CD4-Positive T-Lymphocytes - immunology; CD8; CD8-Positive T-Lymphocytes - immunology; Chronic obstructive pulmonary disease; Chronic obstructive pulmonary disease, asthma; COPD; Disease; Forced Expiratory Volume; Humans; IL4; INF γ; Inflammation; Interferon-gamma - biosynthesis; Interleukin-4 - biosynthesis; Lymphocyte Count; Lymphocytes; Male; Medical sciences; Middle Aged; Nitric oxide; Pathogenesis; Pneumology; Pulmonary Disease, Chronic Obstructive - immunology; Pulmonary Disease, Chronic Obstructive - physiopathology; Smoking; Smoking - immunology; Sputum - cytology; Studies; T-Lymphocyte Subsets - immunology; T-lymphocytes; Tobacco, tobacco smoking; Toxicology; IL4; T-lymphocytes; Pathogenesis; CD8; Chronic obstructive pulmonary disease; Inflammation; INF γ; COPD; Smoking; Lung disease; Respiratory disease; Tobacco smoking; Cell subpopulation; INFγ; Chronic; Sputum; T-Lymphocyte; Bronchus disease; Obstructive pulmonary disease; Pneumology
• ISSN: 0954-6111; 1532-3064
• DOI: 10.1016/j.rmed.2003.08.007

Background: Previous studies have shown that the inflammatory response to cigarette smoking differs between smokers who develop chronic obstructive pulmonary disease (COPD) and those who do not and that the CD8 + T-lymphocytes have been identified as a key player in this process. The aim of this study was to investigate further the role of CD8 + cells and their subtypes in sputum cells. Methods: Sputum induction was performed in 36 COPD patients, 25 smokers without COPD and 10 non-smoking healthy controls. After stimulation of sputum lymphocytes with phorbol-myristate-acetate, we used double immunocytochemical methods to identify CD4 +, CD8 + cells and CD8 + INF γ or IL4 cells (T c1,T c2). Results: COPD patients had an increased number of CD8 + cells in sputum as compared with smokers without COPD ( P=0.0001) and control subjects ( P=0.001). CD8 +-IL4 cells were reduced both in COPD and in smokers without COPD compared to controls ( P=0.0001), while CD8 +-IFN γ cells were significantly reduced only in COPD ( P=0.001) as compared with controls. A significant ( P=0.02) relationship between the CD8 +-IL4/CD8 +-IFN γ ratio and FEV 1 (% pred) was found only in COPD patients. Conclusion: These findings suggest that an imbalance both in T-lymphocyte subpopulation (CD4/CD8) and in CD8 + cell subsets (T c1/T c2) characterizes the inflammatory responses of smokers with established COPD.