ABSTRACT
Asthma is a chronic inflammatory disease characterized by airflow obstruction, airway hyperresponsiveness, and, importantly, the infiltration of lymphocytes, eosinophils, and mast cells, which are believed to be responsible for the physiological manifestations and accompanying airway remodeling. Over a decade of research and clinical efforts have implicated numerous mediators and mechanisms to play a role in the pathogenesis of asthma. The results of studies in animals, particularly in mice, suggest that redundant mechanisms may lead to a similar outcome—asthmatic disease. Delineating the mediators of allergic asthma in animal models is important but is useful only if these studies have relevance to the pathogenesis of human asthma. To delineate such relevance of murine studies, it is important to understand the inherent differences between experimentally induced allergic pulmonary disease in mice and clinical disease in human asthmatics and appreciate the different pathogenic mechanisms that can occur between mice and humans.
