Clinical and immunoregulatory effects of roxithromycin therapy for chronicrespiratory tract infection

Citation
H. Nakamura et al., Clinical and immunoregulatory effects of roxithromycin therapy for chronicrespiratory tract infection, EUR RESP J, 13(6), 1999, pp. 1371-1379
Citations number
34
Categorie Soggetti
Cardiovascular & Respiratory Systems","da verificare
Journal title
EUROPEAN RESPIRATORY JOURNAL
ISSN journal
09031936 → ACNP
Volume
13
Issue
6
Year of publication
1999
Pages
1371 - 1379
Database
ISI
SICI code
0903-1936(199906)13:6<1371:CAIEOR>2.0.ZU;2-I
Abstract
The clinical and immunoregulatory effects of long-term macrolide antibiotic therapy for patients with chronic lower respiratory tract infections (CLRT I) were investigated. Clinical parameters and neutrophil chemotactic mediators in the epithelial lining fluid (ELF) of CLRTI patients (n=10) were examined before and after 3 months oral administration of roxithromycin (RXM), The in vitro effects o f RXM were also examined on the release of these mediators from alveolar ma crophages (AM) and neutrophils. Arterial oxygen tension (p<0.05), vital capacity (VC) (p<0.001), %VC (p<0.0 5) and forced expiratory volume in one second (p<0.01) were improved after RXM treatment, but airway bacteria were not eradicated. Among the mediators , the levels of interleukin (1L)-8, neutrophil elastase (NE) and leukotrien e B-4 (LTB4) were higher in ELF than in plasma of CLRTI patients and they d ecreased after RXM treatment (n=7, p<0.05 for each). RXM concentrations wer e significantly increased in the bronchoalveolar lavage cells of the treate d patients. In in vitro experiments, RXM showed inhibitory effects on IL-8 release from AM and neutrophils. In conclusion, interleukin-8, neutrophil elastase and leukotriene B-4 contr ibute to the neutrophilic inflammation in the airways of chronic lower resp iratory tract infection patients and the clinical effects of roxithromycin may, in part, be attributable to the suppression of excess release of the c hemotactic mediators from inflammatory cells.