Tuberc Respir Dis.  2004 Dec;57(6):543-552. 10.4046/trd.2004.57.6.543.

Effects of CpG-oligodeoxynucleotides in Chronic Inflammation and Remodeling of Airway in a Murine Model of Bronchial Asthma

Affiliations
  • 1Department of Internal Medicine, The Catholic University of Korea, Seoul, Korea. chihongk@yahoo.co.kr
  • 2Research Institute of Medical Science, St. Vincent Hospital, Suwon, Korea.

Abstract

BACKGROUND: Airway remodeling of the asthmatic airway, the result of persistent inflammation in the bronchial wall, is associated with irreversible airway obstruction and the severity of asthma. Previous reports had represented that adminitering CpG-oligodeoxynucleotides (CpG-ODN) before sensitization or challenge by allergens inhibits the development of eosinophilic airway inflammation in a murine model of asthma, but the effects of CpG-ODNs on chronic inflammation and airway remodeling had not been characterized. To investigate the influence of CpG-ODNs on chronic inflammation and remodeling of the airway, we performed studies using a murine model of chronic allergen-induced asthma.
METHODS
Balb/C mice were sensitized to ovalbumin(OVA) and subsequently exposed to nebulized OVA by means of inhalation twice weekly for 7 weeks. CpG-ODNs(30 microgram) was administered intraperitoneally at sensitization. After final inhalation, mice were evaluated for airway hyperresponsiveness, chronic airway inflammation and remodeling.
RESULTS
The mice exposed to chronic and recurrent airway challenge with OVA had persistent airway hyperresponsiveness, chronic inflammation and airway remodeling. Mice treated with CpG-ODNs exhibited decreased bronchial hyperresponsiveness, OVA-specific IgE, chronic inflammation and evidence of airway remodeling, including goblet cell hyperplasia and subepithelial fibrosis.
CONCLUSION
CpG-ODNs was thought to prevent chronic inflammation and remodeling changes in a murine model of chronic asthma.

Keyword

CpG-oligodeoxynucleotides; airway remodeling; murine model of asthma

MeSH Terms

Airway Obstruction
Airway Remodeling
Allergens
Animals
Asthma*
Eosinophils
Fibrosis
Goblet Cells
Hyperplasia
Immunoglobulin E
Inflammation*
Inhalation
Mice
Ovum
Allergens
Immunoglobulin E
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