Open AccessClinical and immunoregulatory effects of roxithromycin therapy for chronic respiratory tract infection
Author(s) -
Nakamura H.,
Fujishima S.,
Inoue T.,
Ohkubo Y.,
Soejima K.,
Waki Y.,
Mori M.,
Urano T.,
Sakamaki F.,
Tasaka S.,
Ishizaka A.,
Kanazawa M.,
Yamaguchi K.
Publication year - 1999
Publication title -
european respiratory journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.021
H-Index - 241
eISSN - 1399-3003
pISSN - 0903-1936
DOI - 10.1034/j.1399-3003.1999.13f23.x
Subject(s) - pneumonia , integrin alpha m , immunosenescence , downregulation and upregulation , medicine , intercellular adhesion molecule 1 , immunology , cell adhesion molecule , flow cytometry , respiratory tract , biology , respiratory system , immune system , biochemistry , gene
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 B 4 (LTB 4 ) 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 B 4 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.