title: A critical role for mouse CXC chemokine(s) in pulmonary neutrophilia during Th type 1-dependent airway inflammation.
abstract: Ag-specific Th1 and Th2 cells have been demonstrated to play a critical role in the induction of allergic diseases. Here we have investigated the precise mechanisms of Th1-induced airway inflammation. Airway inflammation was induced in BALB/c mice by transfer of freshly induced OVA-specific Th1 or Th2 cells followed by OVA inhalation. In this model, both Th1 and Th2 cells induced airway inflammation. The former induced neutrophilia in airways, whereas the latter induced eosinophilia. Moreover, we found that Th1 cells induced more severe airway hyperresponsiveness (AHR) than Th2 cells. The eosinophilia induced by Th2 cell infusion was almost completely blocked by administration of anti-IL-5 mAb, but not anti-IL-4 mAb. In contrast, Th1-induced AHR and pulmonary neutrophilia were inhibited by the administration of anti-human IL-8R Ab, which blocks the function of mouse CXC chemokine(s). These findings reveal a critical role of mouse CXC chemokine(s) in Th1-dependent pulmonary neutrophilia and AHR.
authors.affiliation: Medicinal Research Laboratory, Taisho Pharmaceutical, Saitama, Japan.
authors.forename: A
authors.initials: A
authors.lastname: Takaoka
authors.forename: Y
authors.initials: Y
authors.lastname: Tanaka
authors.forename: T
authors.initials: T
authors.lastname: Tsuji
authors.forename: T
authors.initials: T
authors.lastname: Jinushi
authors.forename: A
authors.initials: A
authors.lastname: Hoshino
authors.forename: Y
authors.initials: Y
authors.lastname: Asakura
authors.forename: Y
authors.initials: Y
authors.lastname: Mita
authors.forename: K
authors.initials: K
authors.lastname: Watanabe
authors.forename: S
authors.initials: S
authors.lastname: Nakaike
authors.forename: Y
authors.initials: Y
authors.lastname: Togashi
authors.forename: T
authors.initials: T
authors.lastname: Koda
authors.forename: K
authors.initials: K
authors.lastname: Matsushima
authors.forename: T
authors.initials: T
authors.lastname: Nishimura
mesh_terms: D000280:Administration, Inhalation; D000336:Aerosols; D000818:Animals; D016535:Bronchial Hyperreactivity / Q000276:immunology / Q000473:pathology; D001992:Bronchoalveolar Lavage Fluid / Q000276:immunology; D019743:Chemokines, CXC / Q000502:physiology*; D004195:Disease Models, Animal; D004804:Eosinophils / Q000276:immunology / Q000473:pathology; D007249:Inflammation / Q000276:immunology; D007964:Leukocytosis / Q000276:immunology* / Q000473:pathology; D008168:Lung / Q000276:immunology* / Q000473:pathology*; D051379:Mice; D008807:Mice, Inbred BALB C; D008822:Mice, Transgenic; D009504:Neutrophils / Q000276:immunology* / Q000473:pathology*; D010047:Ovalbumin / Q000008:administration & dosage / Q000276:immunology; D010446:Peptide Fragments / Q000008:administration & dosage / Q000276:immunology; D012130:Respiratory Hypersensitivity / Q000276:immunology / Q000473:pathology; D018417:Th1 Cells / Q000276:immunology* / Q000637:transplantation; D018418:Th2 Cells / Q000276:immunology / Q000637:transplantation
chemical_list: D000336:Aerosols; D019743:Chemokines, CXC; C111390:OVA 323-339; D010446:Peptide Fragments; D010047:Ovalbumin