In vivo airway eosinophil accumulation does not enhance antigen- or propranolol-induced bronchoconstriction in guinea pigs

Background: Chronic airway eosinophil accumulation is characteristic of asthma. However, it remains unclear whether airway eosinophils enhance or reduce release of chemical mediators and/or action of the released mediators in the airways in vivo, because previous investigators have indicated that eo...

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Bibliographic Details
Published in:Prostaglandins & other lipid mediators 1999-11, Vol.58 (5), p.219-230
Main Authors: Ishiuraa, Yoshihisa, Fujimura, Masaki, Myou, Shigeharu, Amemiya, Tokunao, Nobata, Kouichi, Liu, Qi, Tachibana, Hideki, Matsuda, Tamotsu
Format: Article
Language:English
Subjects:
Administration, Inhalation
Administration, Intranasal
Airway eosinophil accumulation
Allergic bronchoconstriction
Animals
Antigens - pharmacology
Asthma - physiopathology
Bronchoconstriction - drug effects
Bronchoconstrictor Agents
Disease Models, Animal
Eosinophils - metabolism
Guinea Pigs
Lipids
Male
Methacholine Chloride - administration & dosage
Mice
Polymyxin B - administration & dosage
Polymyxin B - pharmacology
Polymyxin-B
Propranolol - pharmacology
Propranolol-induced bronchoconstriction
Respiratory System - cytology
Respiratory System - physiopathology
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Summary:Background: Chronic airway eosinophil accumulation is characteristic of asthma. However, it remains unclear whether airway eosinophils enhance or reduce release of chemical mediators and/or action of the released mediators in the airways in vivo, because previous investigators have indicated that eosinophil-derived factors such as histaminase and arylsulfatase may alter the allergic reaction by metabolizing chemical mediators. Recently, we have developed a guinea pig model of propranolol-induced bronchoconstriction (PIB), which is mediated by lipid mediators such as thromboxane A 2 (TxA 2), cysteinyl leukotrienes (cLTs) and platelet activation factor (PAF). This study was conducted to explain the influence of airway eosinophil accumulation on antigen-induced bronchoconstriction and the following PIB, both of which are mediated by lipid mediators. Methods: Guinea pigs were transnasally treated with 75 μg/kg of polymyxin-B or vehicle twice a week for a total of 3 weeks. Guinea pigs were anesthetized and treated with diphenhydramine hydrochloride, and then artificially ventilated 24 h after the last administration of polymyxin-B or vehicle followed by passive sensitization. Propranolol at a concentration of 10 mg/ml was inhaled 20 min after an aerosolized antigen challenge. Results: The proportion of eosinophils in bronchoalveolar lavage fluid obtained 15 min after the propranolol inhalation was significantly increased in guinea pigs treated with polymyxin-B compared with the vehicle. The polymyxin-B treatment did not affect antigen-induced bronchoconstriction or the following PIB. Conclusions: We conclude that eosinophils accumulated in the airways by polymyxin-B does not affect release of chemical mediators induced by antigen or propranolol inhalation, or action of released mediators in vivo.
ISSN:1098-8823
DOI:10.1016/S0090-6980(99)00040-4