Abstract
Asthma is a significant heterogeneous disease with a high prevalence in
children and adults. The main manifestations of asthma include wheezing, cough,
dyspnea, chest tightness, mucus hypersecretion, and airway hyperresponsiveness to
inhaled allergens with varying degrees of expiratory airflow limitation. Asthma is
mainly considered as a state of dysregulated Th2 immune responses. However, clinical
findings indicate that asthma is a heterogeneous disease with diverse phenotypes,
endotypes and inflammatory cascades. Animal models are critical to advance insights
into the pathophysiology underlying asthma development and to validate the safety and
efficacy of novel therapeutics. Allergic asthma is mostly induced in murine models
through sensitization of mice by one of the two main allergens: ovalbumin and house
dust mite. Murine models were the most used model to investigate immune responses
and genetic background of asthma as well as the basis of the heterogenous
phenotypes/endotypes of the disease. Murine models have also been used to validate
novel therapeutics. While murine models have offered a better understanding of certain
pathways and reactants in the pathogenesis of asthma and airway remodeling, none of
the current models entirely reflect the same features of human asthma. Therefore, great
caution should be considered regarding the extrapolation of data derived from the
murine asthma model to human asthma as they have many limitations and only partly
reflect the pathology of human diseases.
Keywords: Allergic, Animal, Airway, Data, Extrapolation, Endotype, Genetic, Limitations, Model, Murine, Non-murine asthma, Phenotype, Remodeling.