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ADAM‐8, a metalloproteinase, drives acute allergen‐induced airway inflammation
Author(s) -
Paulissen Geneviève,
Rocks Natacha,
Guéders Maud M.,
Bedoret Denis,
Crahay Céline,
QuesadaCalvo Florence,
Hacha Jonathan,
Bekaert Sandrine,
Desmet Christophe,
Foidart JeanMichel,
Bureau Fabrice,
Noel Agnès,
Cataldo Didier D.
Publication year - 2011
Publication title -
european journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.272
H-Index - 201
eISSN - 1521-4141
pISSN - 0014-2980
DOI - 10.1002/eji.200940286
Subject(s) - inflammation , immunology , ovalbumin , allergen , eosinophil , ccl11 , allergic inflammation , chemokine , biology , allergy , eotaxin , asthma , antigen
Abstract 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.