[Eosinophilia and interleukin-5: role in pulmonary atopic processes]

Infiltration of some tissues including the lung by activated eosinophil leukocytes is a characteristic feature of allergic disorders. In asthma patients, eosinophils have been shown to promote and prolong inflammation of bronchial mucosa. This effect is due to the release by eosinophils of numerous inflammation-stimulating mediators and cytokines as well as cationic proteins known to damage lung epithelium. Differentiation of eosinophils from their hematopoietic precursors as well as subsequent processes including maturation, chemotaxis, and activation are controlled mainly by interleukin-5 (IL-5). This cytokine is produced not only by a subpopulation of T-lymphocyte helpers, named Th2, but also by mastocytes and eosinophils themselves. A massive increase in IL-5 concentrations as well as in mRNA for IL-5 synthesis has been detected in serum, broncho-alveolar lavage fluid, and bronchial mucosa of asthmatic patients. In animal models mimicking clinical manifestations of lung allergy, neutralization of IL-5 using specific antibodies inhibits eosinophilic infiltration into the airways and improves respiratory function. These findings suggest that release of IL-5 during atopic disorders is a cardinal step in the development of inflammation and lesions in asthmatic patients. Treatment with drugs that selectively inhibit the synthesis and/or effects of IL-5 could represent a new therapeutic strategy not only for allergic disorders but also for other diseases associated with blood and tissue eosinophilia.