Eosinophilic airway inflammation induced by repeated exposure to cigarette smoke

K. Matsumoto, H. Aizawa, H. Inoue, H. Koto, S. Takata, M. Shigyo, H. Nakano, N. Hara

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Abstract

Acute exposure to cigarette smoke causes airway hyperresponsiveness (AHR) in guinea-pigs, which resolves within a few hours. Repeated exposure may have a different effect on the airways. To address this question, guinea- pigs were repeatedly exposed to cigarette smoke (six cigarettes for 1 h·day-1) for 14 consecutive days. Airway responsiveness to inhaled histamine and differential cell counts in bronchoalveolar lavage fluid (BALF) were evaluated 1 day after the last exposure. Significant neutrophilia in BALF was observed after 3 days of smoke exposure. Significant eosinophilia in BALF and AHR were observed after 14 days of smoke exposure, but not after 3 or 7 days of smoke exposure. These changes persisted until 3 days after the last exposure and resolved 7 days afterwards. Histologically, the recruited eosinophils were observed predominantly in the airways, but not in the alveoli. Treatment with E-6123, a specific platelet-activating factor receptor antagonist (1 mg·kg-1·day-1 p.o. during smoke exposure) significantly inhibited the eosinophil influx and AHR. Repeated exposure to cigarette smoke may induce prolonged airway inflammation and airway hyperresponsiveness in guinea-pigs. Platelet-activating factor or platelet- activating factor-like lipids may play a key role in airway hyperresponsiveness, presumably by the induction of eosinophilic airway inflammation.

Original languageEnglish
Pages (from-to)387-394
Number of pages8
JournalEuropean Respiratory Journal
Volume12
Issue number2
DOIs
Publication statusPublished - Aug 1998

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All Science Journal Classification (ASJC) codes

  • Pulmonary and Respiratory Medicine

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