Heme oxygenase-1 (HO-1) protein induction in a mouse model of asthma

Citation
O. Kitada et al., Heme oxygenase-1 (HO-1) protein induction in a mouse model of asthma, CLIN EXP AL, 31(9), 2001, pp. 1470-1477
Citations number
39
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Clinical Immunolgy & Infectious Disease",Immunology
Journal title
CLINICAL AND EXPERIMENTAL ALLERGY
ISSN journal
0954-7894 → ACNP
Volume
31
Issue
9
Year of publication
2001
Pages
1470 - 1477
Database
ISI
SICI code
0954-7894(200109)31:9<1470:HO(PII>2.0.ZU;2-4
Abstract
Background and objective Carbon monoxide (CO) is known to be present in mea surable 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 refl ects inflammation of the asthmatic airway. Heme oxygenase-1 (HO-1) protein, also called HSP32, is the rate-limiting enzyme in the catabolism of heme t o biliverdin, free iron and CO. However, it is unknown whether an expressio n 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 lava ge cells in a mouse model of asthma. Methods Ovalbumin (OVA)-sensitized C57BL/6 mice were challenged with aeroso lized OVA. HO-1 positive cells were identified by immunostaining in lung ti ssue and bronchoalveolar lavage fluid (BALF) after the challenge. Results HO-1 positive cell numbers increased in the subepithelium of the br onchi after OVA challenge. In cytospin preparations from BALF after OVA cha llenge, HO-1 was localized to alveolar macrophages. Inside the macrophages, HO-1 reactivity was expressed in the cytoplasm, and the perinuclear region in particular. Conclusion The expression of HO-1 is increased within the lung tissue in al lergic airway inflammation. Measurement of HO-1 activity may be clinically useful in the management of asthma.