title: Allergic bronchial asthma: airway inflammation and hyperresponsiveness.
abstract: The international consensus report on diagnosis and treatment of asthma was published in 1992 (Clin Exp Allergy 22: 1-72). According to the report, asthma is a chronic inflammatory disorder of the airways in which many cells play a role, including mast cells and eosinophils. Airway inflammation causes various symptoms of asthma which are usually associated with widespread but variable airflow obstruction and causes an associated increase in airway responsiveness to a variety of stimuli. The definition of asthma, provided in this report, is an epoch-making revision of the conventional recognition of asthma based on respiratory physiology and does not contradict the empirical knowledge that asthma responds well to steroid therapy. One reason, which led airway inflammation to be understood as a major factor in the pathophysiology of asthma is the technological advance and the widespread use of bronchoscopes. The use of bronchoscopy as a research tool has markedly improved the understanding of the pathology of asthma. It became also possible to link biopsy findings to autopsy findings in patients who died of asthma. However, it is relatively difficult to repeat a biopsy of the airway mucosal membranes in individual asthmatic patients. Here, animal models of asthma play a significant role. Findings from animal models can provide a clue for the development of new anti-asthmatic drugs. This paper will deal with the paradigm of allergic asthma and focus on recent topics of interleukin (IL)-4 and IL-5, which seem to play a central role in allergic asthma. The causative relationship between airway inflammation and hyperresponsiveness will be discussed.
authors.affiliation: Medical Imaging Center, Hyogo College of Medicine, Hyogo.
authors.forename: Minoru
authors.initials: M
authors.lastname: Sugita
authors.forename: Kozo
authors.initials: K
authors.lastname: Kuribayashi
authors.forename: Takayuki
authors.initials: T
authors.lastname: Nakagomi
authors.forename: Shigeru
authors.initials: S
authors.lastname: Miyata
authors.forename: Tomohiro
authors.initials: T
authors.lastname: Matsuyama
authors.forename: Osamu
authors.initials: O
authors.lastname: Kitada
mesh_terms: D000402:Airway Obstruction / Q000209:etiology / Q000276:immunology; D000818:Animals; D018927:Anti-Asthmatic Agents / Q000627:therapeutic use; D001249:Asthma / Q000150:complications / Q000276:immunology*; D001980:Bronchi / Q000276:immunology / Q000473:pathology*; D016535:Bronchial Hyperreactivity / Q000209:etiology / Q000276:immunology*; D004802:Eosinophilia / Q000150:complications / Q000276:immunology; D006801:Humans; D006967:Hypersensitivity / Q000150:complications / Q000276:immunology*; D007249:Inflammation / Q000276:immunology* / Q000473:pathology; D015847:Interleukin-4 / Q000276:immunology; D015848:Interleukin-5 / Q000276:immunology; D051379:Mice; D023421:Models, Animal
chemical_list: D018927:Anti-Asthmatic Agents; D015848:Interleukin-5; D015847:Interleukin-4