IL-5-induced airway eosinophilia - the key to asthma?

Bronchial asthma is a chronic inflammatory airway disease defined by revers ible airway obstruction and non-specific airway hyper-responsiveness (AHR), Although profound insights have been made into the pathophysiology of asth ma, the exact mechanisms inducing and regulating the disease are still not fully understood. Yet, it is generally accepted that the pathological chang es in asthma are induced by a chronic inflammatory process which is charact erized by infiltration of the bronchial mucosa with lymphocytes and eosinop hils, increased mucus production and submucosal edema. There is increasing evidence that an imbalance in the T-helper (Th) cell response of geneticall y predisposed individuals to common environmental antigens plays a pivotal role in the pathogenesis of allergic bronchial asthma and other atopic diso rders. Following allergic sensitization, T cells from atopic patients tend to produce elevated levels of Th2-type cytokines, especially interleukin (I L)-4, IL-13, IL-5 and IL-6, which induce and regulate IgE production and eo sinophil airway infiltration. In this review, the role of Th2-type cytokine s, IgE and airway eosinophils in the induction of airway inflammation and A HR is discussed, and animal studies of asthma and AHR, mainly in rodents wi ll be considered. A better understanding of the underlying mechanisms leadi ng to asthma pathology may yield more specific immunological strategies for the treatment of this disease which is increasing worldwide.