title: IL-5 release of CD4+ non-effector lymphocytes is increased in COPD--modulating effects of moxifloxacin and dexamethasone.
abstract: 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.
authors.affiliation: Department of Pneumology, Clinic III for Internal Medicine, University of Cologne, Cologne, Germany.
authors.forename: Katharina
authors.initials: K
authors.lastname: Schild
authors.forename: Jürgen
authors.initials: J
authors.lastname: Knobloch
authors.forename: Yakup
authors.initials: Y
authors.lastname: Yakin
authors.forename: David
authors.initials: D
authors.lastname: Jungck
authors.forename: Katja
authors.initials: K
authors.lastname: Urban
authors.forename: Katja
authors.initials: K
authors.lastname: Müller
authors.forename: Andrea
authors.initials: A
authors.lastname: Koch
mesh_terms: D001372:Aza Compounds / Q000494:pharmacology*; D015496:CD4-Positive T-Lymphocytes / Q000187:drug effects / Q000276:immunology*; D016022:Case-Control Studies; D003907:Dexamethasone / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D005260:Female; D024841:Fluoroquinolones; D006801:Humans; D007155:Immunologic Factors / Q000494:pharmacology*; D015848:Interleukin-5 / Q000096:biosynthesis* / Q000276:immunology; D008297:Male; D008875:Middle Aged; D000077266:Moxifloxacin; D029424:Pulmonary Disease, Chronic Obstructive / Q000097:blood / Q000188:drug therapy / Q000276:immunology*; D011804:Quinolines / Q000494:pharmacology*; D012907:Smoking / Q000097:blood / Q000276:immunology; D018418:Th2 Cells / Q000187:drug effects / Q000276:immunology
chemical_list: D001372:Aza Compounds; D024841:Fluoroquinolones; C508599:IL5 protein, human; D007155:Immunologic Factors; D015848:Interleukin-5; D011804:Quinolines; D003907:Dexamethasone; D000077266:Moxifloxacin