ABSTRACT
Allergic asthma is a complex chronic inflammatory disease of the airways, and its etiology is multifactorial. It involves the recruitment and activation of many inflammatory and structural cells, all of which release inflammatory mediators that result in pathological changes typical of asthma (Barnes et al., 1998; O’Byrne and Postma, 1999). Several features of asthma can be suitably investigated in animal models. These features include cellular infiltrations in the lung, antigen-specific IgE production, and a predominant Th2-type immune response characterized by elevations in the levels of typical cytokines seen upon allergen (hapten) sensitization and challenge. The number of mediators involved in the process of sensitization to an allergen and/or the development of a chronic inflammatory process in the mucosa of the lower airways, including airway remodeling, indicates that these pr ocesses are extremely complex.
