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van der Kleij, H.P. et al.

van der Kleij, Kraneveld, van Houwelingen, Kool, Weitenberg, Redegeld, Nijkamp,

Murine model for non-IgE-mediated asthma.

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.[1]

References

Murine model for non-IgE-mediated asthma. van der Kleij, H.P., Kraneveld, A.D., van Houwelingen, A.H., Kool, M., Weitenberg, A.C., Redegeld, F.A., Nijkamp, F.P. Inflammation (2004) [Pubmed]

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