title: Disruption of antigen-induced airway inflammation and airway hyper-responsiveness in low affinity neurotrophin receptor p75 gene deficient mice.
abstract: 1. Recently, much attention has been paid to the relationship between the nervous and immune systems. The present study was conducted to clarify the role of neurotrophin low affinity receptor (p75N) in allergic airway inflammation and hyper-responsiveness (AHR) in mice by employing p75N gene deficient mice. 2. Mice were immunized twice by intraperitoneal injections of ovalbumin (OA) at intervals of 12 days. OA was inhaled 10 days after the secondary immunization and repeated three times at 4 days interval. Twenty-four hours after the last inhalation, airway responsiveness to acetylcholine was measured and bronchoalveolar lavage fluid (BALF) was obtained for examining the number of inflammatory cells and the level of cytokines. Serum immunoglobulin was measured as a marker of systemic immune response before the final inhalation. 3. In wild-type mice, repeated antigen provocation resulted in airway eosinophilia, AHR and elevations in serum IgE and interleukin (IL)-4 and -5 in BALF. In p75N gene deficient mice, none of the above parameters was observed after antigen provocation. The antigen-induced production of interferon (IFN)-gamma and nerve growth factor (NGF) were not altered by depletion of p75N gene. 4. The present findings suggest that p75 gene deficiency disrupt an allergic airway inflammation and AHR in mice by interfering type 2 helper T (Th2) cell responses.
authors.affiliation: Department of Pharmacology, Gifu Pharmaceutical University, 5-6-1 Mitahora-higashi, Gifu 502-8585, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Tokuoka
authors.forename: Y
authors.initials: Y
authors.lastname: Takahashi
authors.forename: T
authors.initials: T
authors.lastname: Masuda
authors.forename: H
authors.initials: H
authors.lastname: Tanaka
authors.forename: S
authors.initials: S
authors.lastname: Furukawa
authors.forename: H
authors.initials: H
authors.lastname: Nagai
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D000941:Antigens / Q000276:immunology*; D016535:Bronchial Hyperreactivity / Q000276:immunology / Q000503:physiopathology*; D001991:Bronchitis / Q000276:immunology / Q000503:physiopathology*; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry / Q000166:cytology; D016084:Bronchoconstriction / Q000187:drug effects; D016207:Cytokines / Q000096:biosynthesis; D004305:Dose-Response Relationship, Drug; D005838:Genotype; D007073:Immunoglobulin E / Q000097:blood / Q000276:immunology; D008168:Lung / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology; D051379:Mice; D008807:Mice, Inbred BALB C; D018345:Mice, Knockout; D020932:Nerve Growth Factor / Q000096:biosynthesis; D010047:Ovalbumin / Q000276:immunology; D020800:Receptor, Nerve Growth Factor; D017475:Receptors, Nerve Growth Factor / Q000172:deficiency / Q000235:genetics / Q000502:physiology*; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D000941:Antigens; D016207:Cytokines; D020800:Receptor, Nerve Growth Factor; D017475:Receptors, Nerve Growth Factor; D014665:Vasodilator Agents; D007073:Immunoglobulin E; D010047:Ovalbumin; D020932:Nerve Growth Factor; D000109:Acetylcholine