title: Transient contribution of mast cells to pulmonary eosinophilia but not to hyper-responsiveness.
abstract: BACKGROUND
  We have recently demonstrated that the transfer of interleukin (IL)-5-producing CD4+ T cell clones into unprimed mice is sufficient for the development ofeosinophilic inflammation in the bronchial mucosa upon antigen inhalation.
  
  
  OBJECTIVE
  The aim of this study was to elucidate the possible contribution of mast cells in eosinophilic inflammation and bronchial hyper-responsiveness (BHR), and to discriminate between the roles of CD4+ T cells and mast cells.
  
  
  METHODS
  Mast cell-deficient mice (WBB6F1-W/Wv) and their congenic normal littermates (WBB6F1-+/+) were immunized with ovalbumin and challenged by inhalation with the relevant antigen.
  
  
  RESULTS
  Airway eosinophilia was induced with equivalent intensity in +/+ and W/Wv mice 6, 24, 96 and 216 h after antigen inhalation. In contrast, 48 h after antigen challenge, eosinophilic infiltration into the bronchial mucosa was significantly less pronounced in W/Wv mice than in +/+ mice. Anti-CD4 monoclonal antibody (mAb), anti-IL-5 mAb, and cyclosporin A were administered next, demonstrating that the airway eosinophilia of W/Wv mice induced 48 h after antigen challenge was almost completely inhibited by each of these three treatments, but that of +/+ mice was significantly less susceptible. Bronchial responsiveness to acetylcholine was increased 48 h after antigen challenge and was not significantly different between +/+ and W/Wv mice. Administration of anti-IL-5 mAb completely inhibited the development of BHR in both +/+ and W/Wv mice.
  
  
  CONCLUSIONS
  These results indicate that, in mice, mast cells do have a supplemental role in the development of pulmonary eosinophilia but not BHR. CD4+ T cells totally regulate these responses by producing IL-5.
authors: Discovery Research Laboratory, Tanabe Seiyaku Co., Ltd, Saitama, Japan. k-ogawa@tanabe.co.jp
authors: K
authors: K
authors: Ogawa
authors: O
authors: O
authors: Kaminuma
authors: H
authors: H
authors: Kikkawa
authors: A
authors: A
authors: Nakata
authors: M
authors: M
authors: Asahina
authors: R W
authors: RW
authors: Egan
authors: K
authors: K
authors: Akiyama
authors: A
authors: A
authors: Mori
mesh_terms: D000280:Administration, Inhalation; D000818:Animals; D000911:Antibodies, Monoclonal / Q000494:pharmacology; D000941:Antigens / Q000008:administration & dosage / Q000276:immunology; D001980:Bronchi / Q000276:immunology / Q000473:pathology; D016535:Bronchial Hyperreactivity / Q000276:immunology / Q000503:physiopathology*; D001992:Bronchoalveolar Lavage Fluid / Q000166:cytology; D015704:CD4 Antigens / Q000276:immunology; D002465:Cell Movement / Q000187:drug effects; D016572:Cyclosporine / Q000494:pharmacology; D004804:Eosinophils / Q000187:drug effects / Q000473:pathology / Q000502:physiology; D007166:Immunosuppressive Agents / Q000494:pharmacology; D015848:Interleukin-5 / Q000276:immunology; D008297:Male; D008407:Mast Cells / Q000502:physiology*; D051379:Mice; D008815:Mice, Inbred Strains; D011657:Pulmonary Eosinophilia / Q000276:immunology / Q000473:pathology / Q000503:physiopathology*; D013997:Time Factors
chemical_list: D000911:Antibodies, Monoclonal; D000941:Antigens; D015704:CD4 Antigens; D007166:Immunosuppressive Agents; D015848:Interleukin-5; D016572:Cyclosporine