| Effects of CpG-oligodeoxynucleotides in Chronic Inflammation and Remodeling of Airway in a Murine Model of Bronchial Asthma. |
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So Hyang Song, Chi Hong Kim, Dong Hwa Han, Seung Joon Kim, Hwa Sik Moon, Jeong Sup Song, Sung Hak Park |
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. |
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| 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. |
| Key Words:
CpG-oligodeoxynucleotides, airway remodeling, murine model of asthma |
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