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Am. J. Respir. Crit. Care Med., Volume 156, Number 1, July 1997, 266-271

Erythromycin Modulates IL-8 Expression in Normal and Inflamed Human Bronchial Epithelial Cells

HAJIME TAKIZAWA, MASASHI DESAKI, TAKAYUKI OHTOSHI, SHIN KAWASAKI, TADASHI KOHYAMA, MAKOTO SATO, MITSURU TANAKA, TSUYOSHI KASAMA, KAZUO KOBAYASHI, JUN NAKAJIMA, and KOJI ITO

Department of Medicine and Physical Therapy, University of Tokyo, School of Medicine, Hongo, Bunkyo-ku, Tokyo; WHO Collaborating Centre, Tokyo Medical College, Nishishinjuku, Shinjuku-ku, Tokyo; The First Department of Internal Medicine, Showa University, School of Medicine, Hatanodai, Shinagawa-ku, Tokyo; Mycobacteriology Laboratory, Leprosy Research Center, National Institute of Infectious Diseases, Higashimurayama, Tokyo; and Department of Thoracic Surgery, University of Tokyo, School of Medicine, Hongo, Bunkyo-ku, Tokyo, Japan

Erythromycin (EM) and its 14-member macrolide analogues have attracted attention for its effectiveness in a variety of airway diseases, including diffuse panbronchiolitis (DPB), sinobronchial syndrome, and chronic sinusitis. However, its mechanisms of action remain unelucidated. We evaluated the effects of several antibiotics on IL-8 expression by normal and transformed human bronchial epithelial cells, an important source of this potent chemokine involved in cell recruitment into the airways. EM and clarithromycin (CAM) uniquely suppressed mRNA levels as well as the release of IL-8 at the therapeutic and noncytotoxic concentrations (% inhibition of IL-8 protein release: 25.0 ± 5.67% and 37.5 ± 8.99%, respectively, at 10-6 M). The other antimicrobes, including a 16-member macrolide josamycin, showed no effect. Bronchial epithelial cells from very peripheral airways as well as from main bronchi were obtained from patients with chronic airway inflammatory diseases, and EM and CAM inhibited IL-8 release from these cells. Among five patients who underwent bronchoscopy before and after macrolide treatment, four showed decreased levels of IL-8 expression in airway epithelium as assessed by reverse transcription and polymerase chain reaction. Our findings showed these 14-member macrolides had inhibitory effect on IL-8 expression in human bronchial epithelial cells, and this new mode of action may have relevance to their clinical effectiveness in airway diseases.




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