title: Heme oxygenase-1 (HO-1) protein induction in a mouse model of asthma.
abstract: OBJECTIVE
  Carbon monoxide (CO) is known to be present in measurable quantities in the exhalation of asthmatic patients. Corticosteroid treatment resulted in a decrease in exhaled CO levels in asthmatic patients, raising the possibility that an increase in exhaled CO concentration reflects inflammation of the asthmatic airway. Heme oxygenase-1 (HO-1) protein, also called HSP32, is the rate-limiting enzyme in the catabolism of heme to biliverdin, free iron and CO. However, it is unknown whether an expression of HO-1 within the lung tissue is related to allergic airway inflammation. We studied the expression of HO-1 in lung tissue and bronchoalveolar lavage cells in a mouse model of asthma.
  
  
  METHODS
  Ovalbumin (OVA)-sensitized C57BL/6 mice were challenged with aerosolized OVA. HO-1 positive cells were identified by immunostaining in lung tissue and bronchoalveolar lavage fluid (BALF) after the challenge.
  
  
  RESULTS
  HO-1 positive cell numbers increased in the subepithelium of the bronchi after OVA challenge. In cytospin preparations from BALF after OVA challenge, HO-1 was localized to alveolar macrophages. Inside the macrophages, HO-1 reactivity was expressed in the cytoplasm, and the perinuclear region in particular.
  
  
  CONCLUSIONS
  The expression of HO-1 is increased within the lung tissue in allergic airway inflammation. Measurement of HO-1 activity may be clinically useful in the management of asthma.
authors.affiliation: Fifth Department of Internal Medicine, Hyogo College of Medicine, Mukogawa-cho, Nishinomiya, Japan.
authors.forename: O
authors.initials: O
authors.lastname: Kitada
authors.forename: T
authors.initials: T
authors.lastname: Kodama
authors.forename: K
authors.initials: K
authors.lastname: Kuribayashi
authors.forename: D
authors.initials: D
authors.lastname: Ihaku
authors.forename: M
authors.initials: M
authors.lastname: Fujita
authors.forename: T
authors.initials: T
authors.lastname: Matsuyama
authors.forename: M
authors.initials: M
authors.lastname: Sugita
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000485:Allergens / Q000009:adverse effects; D000818:Animals; D001249:Asthma / Q000276:immunology* / Q000378:metabolism*; D001980:Bronchi / Q000166:cytology / Q000187:drug effects; D001985:Bronchial Provocation Tests; D004195:Disease Models, Animal; D004790:Enzyme Induction / Q000502:physiology; D006419:Heme Oxygenase (Decyclizing) / Q000096:biosynthesis* / Q000187:drug effects*; D006420:Hemeproteins / Q000187:drug effects* / Q000378:metabolism*; D007962:Leukocytes / Q000187:drug effects; D008297:Male; D051379:Mice; D010047:Ovalbumin / Q000009:adverse effects; D012965:Sodium Chloride / Q000494:pharmacology; D013601:T-Lymphocytes / Q000187:drug effects; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D000485:Allergens; D006420:Hemeproteins; D014665:Vasodilator Agents; D012965:Sodium Chloride; D010047:Ovalbumin; D006419:Heme Oxygenase (Decyclizing); D000109:Acetylcholine