期刊
EUROPEAN JOURNAL OF IMMUNOLOGY
卷 41, 期 2, 页码 380-391出版社
WILEY
DOI: 10.1002/eji.200940286
关键词
ADAM; Asthma; CCL22; DC; Inflammation
类别
资金
- Communaute francaise de Belgique (Actions de Recherches Concertees)
- Fonds de la Recherche Scientifique Medicale
- Fonds National de la Recherche Scientifique (F.N.R.S., Belgium)
- Fonds speciaux de la Recherche (University of Liege)
- Fondation Leon Fredericq (University of Liege)
- Region Wallonne (Belgium)
- European Union
- Interuniversity Attraction Poles Program - Belgian Science Policy IUAP program (Brussels, Belgium) [35]
Asthma is a complex disease linked to various pathophysiological events including the activity of proteinases. The multifunctional A disintegrin and metalloproteinases (ADAMs) displaying the ability to cleave membrane-bound mediators or cytokines appear to be key mediators in various inflammatory processes. In the present study, we investigated ADAM-8 expression and production in a mouse model of allergen-induced airway inflammation. In allergen-exposed animals, increased expression of ADAM-8 was found in the lung parenchyma and in DC purified from the lungs. The potential role of ADAM-8 in the development of allergen-induced airway inflammation was further investigated by the use of an anti-ADAM-8 antibody and ADAM-8 knockout animals. We observed a decrease in allergen-induced acute inflammation both in BALF and the peribronchial area in anti-ADAM-8 antibody-treated mice and in ADAM-8-deficient mice (ADAM-8(-/-)) after allergen exposure. ADAM-8 depletion led to a significant decrease of the CD11c(+) lung DC. We also report lower levels of CCL11 and CCL22 production in antibody-treated mice and ADAM-8-deficient mice that might be explained by decreased eosinophilic inflammation and lower numbers of DC, respectively. In conclusion, ADAM-8 appears to favour allergen-induced acute airway inflammation by promoting DC recruitment and CCL11 and CCL22 production.
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