ABSTRACT
BACKGROUND: COPD is a major global health problem affecting 4-10% of Indian adult male population. Immunological processes have been implicated in the pathogenesis of COPD. As compared to healthy smokers, COPD patients have airway inflammation indicated by the presence of CD8+ T cells in the lung. This predominant increase in CD8+ T cells in the lung may be reflected in the peripheral blood. In an attempt to understand why only some smokers develop COPD, we compared the peripheral T-cell markers in COPD patients with that of asymptomatic smokers, and healthy nonsmokers. METHODS: Twenty healthy non-smokers (HNS), 19 asymptomatic smokers (AS) and 21 COPD male patients (age and pack year-matched) were identified after clinical evaluation and spirometry. Blood CD3+, CD4+, CD8+ T-cell populations were measured. RESULTS: Smokers with COPD had severe airflow limitation (FVC, 69.8+16.7%; FEV1, 47.47+16.9%; FEV1/FVC, 53.1+13.3%). The BMI was found to be significantly lower among patients with COPD (19.1+4.8kg/m(2)) as compared to AS (23+4.3kg/m(2)) and HNS (23.7+4.0kg/m(2)) (p value = 0.003 HS). The mean CD3+T-cell absolute count in COPD patients (1154.3+582.2), showed a marked decline as compared to that of AS (1251.9+491.6) and HNS (1424.9+352.2). The mean CD4+T-cell counts in COPD patients (652.7+340.5) were also lower when compared to AS (745.7+313.8) and HNS (832.5+220.7). The mean CD8+T-cell counts among COPD patients (424.7+264.3) were, similar to the counts observed among AS (426.9+193.2) and HNS (500.4+191). Though not statistically significant, the absolute counts of CD3+, CD4+ and CD8+ lymphocytes among COPD patients tended to be lower. No significant difference in the CD4+/CD8+ lymphocyte ratio between the patient groups was observed. CONCLUSION: Our study indicates that BMI is related to the severity of COPD, hence proving a systemic component to its pathogenesis. However, we found similar percentages of CD8+Tcells in all the study groups suggesting that predominant CD8+ T cells in the airways may be due to its de novo origin rather than recruitment from blood. However, larger studies are needed to clarify the effect of disease severity, beedi smoking and ethnicity.
