Interleukin-5 as a potential target for asthma treatment

Increased accumulation of eosinophils in bronchial mucosa is a hallmark of bronchial asthma. Upon activation, these eosinophils synthesize and release an array of proinflammatory and cytotoxic products that cause edema, mucus secretion, tissue damage and airway hyperreactivity. Maturation, activation and survival of eosinophils are largely dependent on the availability of the hematopoietic cytokine interleukin-5 (IL-5), produced by activated T-helper type 2 (Th2) lymphocytes. Numerous findings obtained in animal models of asthma, utilizing IL-5 transgenic mice or anti-IL-5 antibodies, have underscored the key contribution of this cytokine to the allergic process. Clinical studies in humans have also indicated the close correlation between airway IL-5 expression, eosinophilia and asthma symptoms. Taken together, these findings have advanced IL-5 to a potentially successful target for asthma treatment. Current tactics to tackle IL-5 are neutralization of IL-5, IL-5 receptor antagonism, interference with IL-5-induced intracellular signaling and inhibition of IL-5 biosynthesis.