title: Roles of basophils and mast cells infiltrating the lung by multiple antigen challenges in asthmatic responses of mice.
abstract: OBJECTIVE
  Mast cell hyperplasia has been observed in the lungs of mice with experimental asthma, but few reports have studied basophils. Here, we attempted to discriminate and quantify mast cells and basophils in the lungs in a murine asthma model, determine if both cells were increased by multiple antigen challenges and assess the roles of those cells in asthmatic responses.
  
  
  METHODS
  Sensitized Balb/c mice were intratracheally challenged with ovalbumin four times. Mast cells and basophils in enzymatically digested lung tissue were detected by flow cytometry. An anti-FcεRI monoclonal antibody, MAR-1, was i.p. administered during the multiple challenges.
  
  
  RESULTS
  The numbers of both mast cells (IgE(+) C-kit(+) ) and basophils (IgE(+) C-kit(-) CD49b(+) ) increased in the lungs after three challenges. Treatment with MAR-1 completely abolished the increases; however, a late-phase increase in specific airway resistance (sRaw), and airway eosinophilia and neutrophilia were not affected by the treatment, although the early-phase increase in sRaw was suppressed. MAR-1 reduced antigen-induced airway IL-4 production. Basophils infiltrating the lung clearly produced IL-4 after antigen stimulation in vitro; however, histamine and murine mast cell protease 1 were not increased in the serum after the challenge, indicating that mast cell activation was not evoked.
  
  
  CONCLUSIONS
  Both mast cells and basophils infiltrated the lungs by multiple intratracheal antigen challenges in sensitized mice. Neither mast cells nor basophils were involved in late-phase airway obstruction, although early-phase obstruction was mediated by basophils. Targeting basophils in asthma therapy may be useful for an early asthmatic response.
authors.affiliation: Department of Pharmacology, Kyoto Pharmaceutical University, Kyoto, Japan. nabe@mb.kyoto-phu.ac.jp
authors.forename: T
authors.initials: T
authors.lastname: Nabe
authors.forename: K
authors.initials: K
authors.lastname: Matsuya
authors.forename: K
authors.initials: K
authors.lastname: Akamizu
authors.forename: M
authors.initials: M
authors.lastname: Fujita
authors.forename: T
authors.initials: T
authors.lastname: Nakagawa
authors.forename: M
authors.initials: M
authors.lastname: Shioe
authors.forename: H
authors.initials: H
authors.lastname: Kida
authors.forename: A
authors.initials: A
authors.lastname: Takiguchi
authors.forename: H
authors.initials: H
authors.lastname: Wakamori
authors.forename: M
authors.initials: M
authors.lastname: Fujii
authors.forename: K
authors.initials: K
authors.lastname: Ishihara
authors.forename: S
authors.initials: S
authors.lastname: Akiba
authors.forename: N
authors.initials: N
authors.lastname: Mizutani
authors.forename: S
authors.initials: S
authors.lastname: Yoshino
authors.forename: D D
authors.initials: DD
authors.lastname: Chaplin
mesh_terms: D000402:Airway Obstruction / Q000276:immunology; D000403:Airway Resistance / Q000276:immunology; D000818:Animals; D000941:Antigens / Q000008:administration & dosage / Q000276:immunology; D001249:Asthma / Q000276:immunology* / Q000378:metabolism; D001491:Basophils / Q000276:immunology* / Q000378:metabolism; D004195:Disease Models, Animal; D005260:Female; D015847:Interleukin-4 / Q000276:immunology; D008168:Lung / Q000276:immunology*; D008407:Mast Cells / Q000276:immunology* / Q000378:metabolism; D051379:Mice; D008807:Mice, Inbred BALB C; D010047:Ovalbumin / Q000008:administration & dosage / Q000276:immunology; D013997:Time Factors
chemical_list: D000941:Antigens; D015847:Interleukin-4; D010047:Ovalbumin