PAF mediates cigarette smoke-induced goblet cell metaplasia in guinea pig airways

Masashi Komori, Hiromasa Inoue, Koichiro Matsumoto, Hiroshi Koto, Satoru Fukuyama, Hisamichi Aizawa, Nobuyuki Hara

Research output: Contribution to journalArticlepeer-review

15 Citations (Scopus)

Abstract

Goblet cell metaplasia is an important morphological feature in the airways of patients with chronic airway diseases; however, the precise mechanisms that cause this feature are unknown. We investigated the role of endogenous platelet-activating factor (PAF) in airway goblet cell metaplasia induced by cigarette smoke in vivo. Guinea pigs were exposed repeatedly to cigarette smoke for 14 consecutive days. The number of goblet cells in each trachea was determined with Alcian blue-periodic acid-Schiff staining. Differential cell counts and PAF levels in bronchoalveolar lavage fluid were also evaluated. Cigarette smoke exposure significantly increased the number of goblet cells. Eosinophils, neutrophils, and PAF levels in bronchoalveolar lavage fluid were also significantly increased after cigarette smoke. Treatment with a specific PAF receptor antagonist, E-6123, significantly attenuated the increases in the number of airway goblet cells, eosinophils, and neutrophils observed after cigarette smoke exposure. These results suggest that endogenous PAF may play a key role in goblet cell metaplasia induced by cigarette smoke and that potential roles exist for inhibitors of PAF receptor in the treatment of hypersecretory airway diseases.

Original languageEnglish
Pages (from-to)L436-L441
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Volume280
Issue number3 24-3
DOIs
Publication statusPublished - Mar 2001
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Physiology
  • Pulmonary and Respiratory Medicine
  • Physiology (medical)
  • Cell Biology

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