Eosinophils play a major role in the onset and maintenance of bronchial inflammation and tissue injury in asthma. Like other leukocytes, eosinophils present in excessive numbers in inflamed tissues are removed by apoptosis. This phenomenon, also called 'programmed cell death', allows elimination of dangerous or redundant cells, thereby ensuring maintenance of tissue homeostasis. It has been suggested that a defect in eosinophil apoptosis would participate in the development and persistence of allergic airways inflammation in asthma. Eosinophil apoptosis, as well as the expression and function of various molecules determining this process, are closely regulated by various stimuli, including cytokines, lipid mediators and growth factors released by various cell types and by the eosinophil itself, as well as exogenous molecules, such as glucocorticoids. These stimuli have been shown to alter the expression and function of different molecules involved in the cascade of events characterising the apoptotic process, particularly Bcl-2 family proteins and the pro-apoptotic membrane glycoprotein, Fas. These observations, together with a better understanding of the mechanisms underlying eosinophil apoptosis, will help to more clearly define the molecular events involved in accumulation of these cells in blood and tissues and to identify potential new targets for the treatment of allergic diseases. (C) 2000 Editions scientifiques et medicales Elsevier SAS.
