title: In vivo airway eosinophil accumulation does not enhance antigen- or propranolol-induced bronchoconstriction in guinea pigs.
abstract: 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 A2 (TxA2), 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 microg/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.
authors.affiliation: The Third Department of Internal Medicine, Kanazawa University School of Medicine, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Ishiura
authors.forename: M
authors.initials: M
authors.lastname: Fujimura
authors.forename: S
authors.initials: S
authors.lastname: Myou
authors.forename: T
authors.initials: T
authors.lastname: Amemiya
authors.forename: K
authors.initials: K
authors.lastname: Nobata
authors.forename: Q
authors.initials: Q
authors.lastname: Liu
authors.forename: H
authors.initials: H
authors.lastname: Tachibana
authors.forename: T
authors.initials: T
authors.lastname: Matsuda
mesh_terms: D000280:Administration, Inhalation; D000281:Administration, Intranasal; D000818:Animals; D000941:Antigens / Q000494:pharmacology*; D001249:Asthma / Q000503:physiopathology; D016084:Bronchoconstriction / Q000187:drug effects*; D016085:Bronchoconstrictor Agents; D004195:Disease Models, Animal; D004804:Eosinophils / Q000378:metabolism*; D006168:Guinea Pigs; D008055:Lipids; D008297:Male; D016210:Methacholine Chloride / Q000008:administration & dosage; D051379:Mice; D011112:Polymyxin B / Q000008:administration & dosage / Q000494:pharmacology; D011433:Propranolol / Q000494:pharmacology*; D012137:Respiratory System / Q000166:cytology* / Q000503:physiopathology
chemical_list: D000941:Antigens; D016085:Bronchoconstrictor Agents; D008055:Lipids; D016210:Methacholine Chloride; D011433:Propranolol; D011112:Polymyxin B