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Murine model for non-IgE-mediated asthma.

Authors :
van der Kleij HP
Kraneveld AD
van Houwelingen AH
Kool M
Weitenberg AC
Redegeld FA
Nijkamp FP
Source :
Inflammation [Inflammation] 2004 Jun; Vol. 28 (3), pp. 115-25.
Publication Year :
2004

Abstract

There is increasing evidence that inflammatory mechanisms other than atopy or eosinophilic inflammation may be involved in the pathogenesis of asthma. The mechanisms associated with non-atopic (non-IgE) or neutrophil-mediated asthma are poorly investigated. Non-atopic airway inflammation and hyperresponsiveness was induced in mice by skin sensitization with dinitrofluorobenzene (DNFB) followed by intra-airway challenge with dinitrobenzene sulfonic acid (DNS). Acute bronchoconstriction and mast cell activation were observed shortly after challenge. Increased levels of the major mast cell mediator, TNF-alpha, were found in the bronchoalveolar lavage fluid of DNFB-sensitized. Mast cells play a key role in the early release of TNF-alpha since mast-cell-deficient WBB6F1-W/Wv mice did not show an increase in TNF-alpha release after DNFB-sensitization and DNS challenge compared to their ++ littermates. Features of the late-phase pulmonary reaction included mononuclear and neutrophilic cell infiltration, pulmonary edema, in vitro tracheal hyperreactivity and in vivo airway hyperresponsiveness. These characteristics bear marked similarity with those observed in non-atopic asthmatic patients. Therefore, this model can be used to further study the mechanisms potentially responsible for the development of non-IgE-mediated asthma.

Details

Language :
English
ISSN :
0360-3997
Volume :
28
Issue :
3
Database :
MEDLINE
Journal :
Inflammation
Publication Type :
Academic Journal
Accession number :
15527166
Full Text :
https://doi.org/10.1023/b:ifla.0000039557.33267.65