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+ INFgamma or IL4 cells (Tc1,Tc2). 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+-IFNgamma 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+-IFNgamma ratio and FEV1 (% 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 (Tc1/Tc2) characterizes the inflammatory responses of smokers with established COPD.
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 COPDpatients, 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+ INFgamma or IL4 cells (Tc1,Tc2). RESULTS:COPDpatients 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+-IFNgamma 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+-IFNgamma ratio and FEV1 (% pred) was found only in COPDpatients. CONCLUSION: These findings suggest that an imbalance both in T-lymphocyte subpopulation (CD4/CD8) and in CD8+ cell subsets (Tc1/Tc2) characterizes the inflammatory responses of smokers with established COPD.
Authors: Dahis Manzanares; Maria Srinivasan; Samuel T Salathe; Pedro Ivonnet; Nathalie Baumlin; John S Dennis; Gregory E Conner; Matthias Salathe Journal: Am J Physiol Lung Cell Mol Physiol Date: 2014-01-10 Impact factor: 5.464
Authors: Jeanine M D'Armiento; Steven M Scharf; Michael D Roth; John E Connett; Andrew Ghio; David Sternberg; Jonathan G Goldin; Thomas A Louis; Jenny T Mao; George T O'Connor; Joe W Ramsdell; Andrew L Ries; Neil W Schluger; Frank C Sciurba; Melissa A Skeans; Helen Voelker; Robert E Walter; Christine H Wendt; Gail G Weinmann; Robert A Wise; Robert F Foronjy Journal: Respir Res Date: 2009-11-19