Asthma is associated with eosinophilic airway inflammation and eosinophils are believed to be important in the pathogenesis of asthma. IL-5 has been considered the central mediator for eosinophilic proliferation, differentiation and eosinophilic inflammation, but results of recent studies suggest that besides IL-5, eotaxin may contribute to the pathogenesis of asthma. Eotaxin is CC chemokine first isolated from guinea pig bronchoalveolar lavage. It selectively binds to a specific receptor (CCR3) highly expressed on eosinophils, basophils, and mast cells being important in the pathogenesis of asthma. Eotaxin is produced mainly by epithelial cells of lung and gut, to mediate organ preferential attraction of eosinophils. Production of eotaxin is stimulated by IL-4, IL-13, TNF(-alpha). Human eotaxin family includes: eotaxin-1 (CCL11), eotaxin-2 (CCL24) and eotaxin-3 (CCL26). It seems that eotaxin-3 may be expressed following allergen challenge. Studies with glucocorticosteroids have shown some inhibitory effect on eotaxin production in cell culture in vitro however, very little in vivo data exists in humans relating to corticosteroid effects on chemokine levels. CCR3 receptor is considered as the possible therapeutic target in asthma treatment.