Journal
INTERNATIONAL IMMUNOPHARMACOLOGY
Volume 11, Issue 4, Pages 444-448Publisher
ELSEVIER
DOI: 10.1016/j.intimp.2010.12.013
Keywords
Lymphocyte; COPD; IL-5; Lipopolysaccharide (LPS); Moxifloxacin
Categories
Funding
- Bayer Vital GmbH Leverkusen, Germany
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T-lymphocytes are crucial in chronic obstructive pulmonary disease (COPD) pathogenesis. Especially T(H)1-lymphocytes are involved in local and systemic inflammation in COPD, yet the role of T(H)2-mediated immune-responses in COPD pathogenesis is poorly understood. The objective of this study was to examine IL-5 expression in T(H)2-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 T(H)2-lymphocytes, IL-5 release increased without differences between the cohorts. LPS reduced IL-5 release of ex vivo generated T(H)2-lymphocytes without differences in all cohorts. Moxifloxacin and dexamethasone significantly reduced IL-5 release in T(H)2-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 T(H)2-based immune responses might be suppressed in response to gram-negative bacterial infections independent from smoking and disease status. Dexamethasone and moxifloxacin both have T(H)2-immunmodulating effects. (C) 2010 Elsevier B.V. All rights reserved.
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