Allergic asthma is a chronic inflammatory disease of the airways characterized by airway inflammation, reversible bronchoconstriction, and airway hyperresponsiveness. Recent advancements lead to the identification of a number of cellular and molecular components that contribute to airway inflammation. Allergic asthma is a disease of the airways characterized by reversible bronchial obstruction and airway hyper responsiveness associated with allergic inflammation. Discovery of the individual molecular and cellular components of asthma has depended heavily on animal models that mimic human disease. In this regard, these models have enabled description of a complex sequence of events involving T cells, B cells, dendritic cells, mast cells, macrophages, eosinophils, epithelial cells, and endothelial cells. Differential responses of these various cell types to triggers of asthma result in a hierarchy of cytokine, chemokine, and mediator release leading to homing and activation of immune and inflammatory cells in the pulmonary vasculature and culminating in allergic inflammation. Some of these cells and molecules are also responsible for development of airway hyper responsiveness. Mouse models are particularly valuable, especially in conjunction with the use of genetically engineered animals with heightened expression or deficiency of certain gene products. This chapter briefly discusses various methodological aspects of mouse models and then reviews some of the critical components in progression of asthma for which the models have provided insights, including cytokine release, mast cell activation and degranulation, and homing of eosinophils.
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