PT  - JOURNAL ARTICLE
AU  - H Nakamura
AU  - S Fujishima
AU  - T Inoue
AU  - Y Ohkubo
AU  - K Soejima
AU  - Y Waki
AU  - M Mori
AU  - T Urano
AU  - F Sakamaki
AU  - S Tasaka
AU  - A Ishizaka
AU  - M Kanazawa
AU  - K Yamaguchi
TI  - Clinical and immunoregulatory effects of roxithromycin therapy for chronic respiratory tract infection
AID  - 10.1183/09031936.99.13613809
DP  - 1999 Jun 01
TA  - European Respiratory Journal
PG  - 1371--1379
VI  - 13
IP  - 6
4099  - http://erj.ersjournals.com/content/13/6/1371.short
4100  - http://erj.ersjournals.com/content/13/6/1371.full
SO  - Eur Respir J1999 Jun 01; 13
AB  - The clinical and immunoregulatory effects of long-term macrolide antibiotic therapy for patients with chronic lower respiratory tract infections (CLRTI) 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 of RXM were also examined on the release of these mediators from alveolar macrophages (AM) and neutrophils. Arterial oxygen tension (p<0.05), vital capacity (VC) (p<0.001), %VC (p<0.05) 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 (IL)-8, neutrophil elastase (NE) and leukotriene B4 (LTB4) were higher in ELF than in plasma of CLRTI patients and they decreased after RXM treatment (n = 7, p<0.05 for each). RXM concentrations were significantly increased in the bronchoalveolar lavage cells of the treated 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 B4 contribute to the neutrophilic inflammation in the airways of chronic lower respiratory tract infection patients and the clinical effects of roxithromycin may, in part, be attributable to the suppression of excess release of the chemotactic mediators from inflammatory cells.