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Asthma is a common syndrome characterized by intermittent, reversible, airflow obstruction that is associated with airway hyperresponsiveness, mucus hypersecretion, and inflammation. With the advent of fiberscopic bronchoscopy, it has become possible to classify the nature of the cellular inflammation present in the airways of asthmatics. The balance of CD4 lymphocyte subsets, Th1 and Th2, is now recognized to be important in the pathogenesis of asthma. CD4 Th2 lymphocytes are central to the disease process and exert their effects through inflammatory cytokines that they release in response to activation by antigen. Th1 cells appear to be protective against the development of the disease. The treatment of asthma has traditionally been focused on decreasing inflammation and maximizing bronchodilation. Steroids and β-agonists have long since been the mainstay of therapy; however, there are now under investigation novel therapies targeted to inhibit specific proinflammatory mediators. Additionally, immunotherapy with repeated low-dose antigen exposure has had some promising results. The future of the treatment of asthma will be dependent on continued investigation into its pathogenesis.
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Whittaker et al. (2002) studied this question.
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