IL-5 release of CD4+ non-effector lymphocytes is increased in COPD - modulating effects of moxifloxacin and dexamethasone

T-lymphocytes are crucial in chronic obstructive pulmonary disease (COPD) pathogenesis. Especially TH1-lymphocytes are involved in local and systemic inflammation in COPD, yet the role of TH2-mediated immune-responses in COPD pathogenesis is poorly understood. The objective of this study was to examine IL-5 expression in TH2-lymphocytes in smokers with and without COPD ex vivo compared with non-smokers and to evaluate the effects of bacterial endotoxin (lipopolysaccharide, LPS) as well as two drugs often used for treatment of COPD exacerbation, corticosteroids and moxifloxacin. CD4+ lymphocytes were isolated from the peripheral blood of non-smokers (NS; n = 11), current smokers without airflow limitation (S; n = 11) and smokers with COPD (n = 11). Baseline IL-5 release of CD4+ T-lymphocytes was significantly increased in COPD compared to S and NS. After T-cell activation and differentiation into TH2-lymphocytes, IL-5 release increased without differences between the cohorts. LPS reduced IL-5 release of ex vivo generated TH2-lymphocytes without differences in all cohorts. Moxifloxacin and dexamethasone significantly reduced IL-5 release in TH2-lymphocytes in the absence and presence of LPS without differences between groups. In summary, our data indicate that IL-5 might contribute to systemic inflammation in smokers with COPD and that TH2-based immune responses might be suppressed in response to gram-negative bacterial infections independent from smoking and disease status. Dexamethasone and moxifloxacin both have TH2-immunmodulating effects.