COPD and macrolide

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.