A20 attenuates allergic airway inflammation in mice.
J Immunol
; 183(2): 1488-95, 2009 Jul 15.
Article
en En
| MEDLINE
| ID: mdl-19553520
ABSTRACT
TNF receptor 1 can activate signaling pathways leading to the activation of NF-kappaB. A20, an NF-kappaB-inducible protein, negatively regulates these signaling pathways and acts as an anti-inflammatory mediator. Therefore, A20 is viewed as a potential therapeutic target for inflammatory disease. In this study, we examined the effect of A20 on an OVA-induced allergic airway inflammation model in mice. We used an adenovirus containing A20 cDNA (Ad-A20) that was delivered intratracheally before OVA challenge. Single administration of Ad-A20 reduced airway inflammatory cell recruitment and peribronchiolar inflammation and suppressed the production of various cytokines in bronchoalveolar fluid. In addition, Ad-A20 suppressed mucus production and prevented the development of airway hyperresponsiveness. The protective effect of Ad-A20 was mediated by the inhibition of the NF-kappaB signaling pathway. Taken together, our results suggest that the development of an immunoregulatory strategy based on A20 may have therapeutic potential for the treatment of allergic asthma.
Texto completo:
1
Banco de datos:
MEDLINE
Asunto principal:
Cisteína Endopeptidasas
/
Hiperreactividad Bronquial
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Péptidos y Proteínas de Señalización Intracelular
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Inflamación
Tipo de estudio:
Prognostic_studies
Límite:
Animals
Idioma:
En
Año:
2009
Tipo del documento:
Article