Animal Models to Study Chemokine Receptor Function In Vivo

Abstract

Animal models using guinea pigs, monkeys, rats, and mice have been employed to study the pathogenesis of asthma. More recently, mouse models of allergic lung disease have been used to dissect the complex pathophysiological mechanisms underlying the asthma phenotype. This increase in usage of mouse models stems from the range of tools available for outlining functional pathways for individual cells and mediators. Genetic technologies allow us to manipulate the expression of particular molecules of interest and, therefore, it is possible to dissect inflammatory pathways to investigate the functional roles of particular mediators or cells. Mice can be induced to display a range of the pathophysiological features that are hallmarks of the human disease, including inflammatory cell recruitment to the lung, mucus secretion from the bronchoepithelial surface, serum IgE, and IgG2a, accompanied by a Th2 cytokine profile. Importantly, these pathophysiological indicators are generally accompanied by changes in lung function, allowing correlation between changes in cell or mediator expression and lung physiology.