Asthma is associated with atopy and recruitment of eosinophils to the airways, leading to the hypothesis that its pathogenesis is driven by a Th2 response to inhaled antigens20). Numerous studies have demonstrated that TNF-α and IL-4 attributes contribute to the inflammatory conditions present in airway of asthmatic subjects. TNF-α is expressed in asthmatic airways and may play a key role in amplifying atopic inflammation through the activation of various transcription factors such as nuclear factor-κB (NF-κB). TNF-α is expressed primarily by the alveolar cells and tissue macrophages, mast cells, and bronchial cells, and increase the production of several chemitaxins21,22). IL-4 is critical for the synthesis of IgE by B lymphocytes and to the development of Th2 cells. IL-4 receptor blocking antibodies inhibit allergen-induced airway hyperresponsiveness and pulmonary eosinophilia in a murine model23). In addition, co-treatment of TNF-α and IL-4 were reported to synergize in the secretion of various chemokines5,23,24). Bisset et al. reported that several chemokines and their receptors involve with pathogenesis of allergic asthma25). Several members of the C-C branch of chemokines exhibit chemoattractant properties toward eosinophils, and these include TARC, eotaxin, and RANTES. Numerous studies suggested that TNFα and IL-4 treatment stimulates production of TARC26), eotaxin24), and RANTES27). Present results also shown that TNFα and IL-4 treatments enhances TARC, eotaxin, and RANTES releases in human bronchial epithelial A549 cells.