Mast cell mouse/human differences

The mouse has commonly been utilized as a model for human asthma. The mouse that can be sensitized to a variety of antigens has proven to be a valuable resource in understanding many components of the pathogenesis of asthma in humans. However, the mouse model is not a perfect model as there are differences in degranulation of eosinophils and release of serotonin from mast cells between mice and humans in the mouse model of asthma compared to human asthma. Transgenic mice may be a valuable asset to utilize in understanding pathways and potential realms for therapeutic intervention. 

The rat is also a common model for human asthma and has a size advantage over the mouse, resulting in enhanced ability for collection of blood and bronchoalveolar fluid. The BN rat is the most commonly utihzed strain due to its pronounced IgE and inflammatory response to challenge following sensitization (Hylkema et al., 2002). As is the case with the mouse, rats are not considered a perfect model due to differences in the release of serotonin from mast cells between rats and humans. 

With these differences in mind, we review some of the important findings identified using mouse models of human asthma with specific emphasis on the role of mast cells and IgE. We present published studies and our own data that investigate the role of mast cells and IgE in murine models of allergic inflammation. Finally, we attempt to interpret and reconcile the disparate murine data and put them in context with recent human trials using an anti-IgE antibody. 

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