COPD and macrolide

Mutsuo Yamaya, Tomoko Suzuki, Kota Ishizawa, Takahiko Sasaki, Hiroyasu Yasuda, Daisuke Inoue, Hiroshi Kubo, Katsutoshi Nakayama, Hidekazu Nishimura, Kiyohisa Sekizawa

Research output: Contribution to journalReview articlepeer-review

Abstract

Respiratory virus including rhinovirus (RV) induces exacerbations of chronic obstructive pulmonary disease (COPD). RV infection stimulates various cells in the airways such as epithelial cells, mast cells and eosinophils, and produces a variety of proinflammatory cytokines such as interleukin (IL)-6 and IL-8, mucin and chemical mediators including histamine. These factors may be associated with airway inflammation with leukocyte accumulation, mucus hypersecretion, airway smooth muscle contraction and subsequent COPD exacerbations with airway narrowing. Macrolide antibiotics bafilomycin A1 and erythromycin inhibit RV infection by reducing the expression of ICAM-1, the major RVs receptor, and by blocking RV entry. Furthermore, erythromycin reduced the frequency of common colds and COPD exacerbations. Erythromycin increases bactericidal activity of airway surface liquid in human airway epithelial cells through human beta-defensin production. Herein, we review the pathogenesis of RV infection-induced exacerbations of COPD. Furthermore, we describe the mechanisms of the inhibitory effects of erythromycin on COPD exacerbations.

Original languageEnglish
Pages (from-to)158-166
Number of pages9
JournalJapan Medical Association Journal
Volume49
Issue number4
Publication statusPublished - 2006 Apr 1

Keywords

  • COPD
  • Cytokine
  • Defensin
  • Macrolide
  • Mucin
  • Rhinovirus

ASJC Scopus subject areas

  • Medicine(all)

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