Objectives: Inhalation of spores from the Aspergillus fumigatus may cause local inflammation. The mucosal surface of the respiratory tract provides host defense mechanism. It is unclear why airway exposure to fungal pathogens leads to Th2 response. We report inhibition of Th1 biased epithelial inflammation by an Aspergillus extract (AE). Methods: Beas2B cells were cultured in a 37°C incubator in media with 5%FBS. Cells were treated with AE for 1h and were then stimulated with the TLR3 activator dsRNA for 6h. RNA was isolated and was reverse transcribed to cDNA. Real-time polymerase chain reaction (PCR) analysis was performed in the presence of specific primers and fluorescently labeled probes. The estimation of cytokines including BAFF and IP-10 was conducted using commercially available kits. Results: We conducted experiments assessing the ability of AE to modulate dsRNA induced expression of Th1 biased chemokines and cytokines by epithelial cells. Expressed genes analyzed included IP-10, BAFF, IFIT-1, and a few other Th-1 biased chemokines. We observed that AE suppressed dsRNA induced expression of mRNA for BAFF and IP-10 in Beas2b cells when compared with control (p<0.001). BAFF and IP-10 protein expression was also significantly suppressed ( P < 0.05). Furthermore we found no alteration of BAFF and IP-10 mRNA expression in Beas2b cells when treated only with the diluent (without AE) and stimulated with dsRNA for 6 hours. We observed increased dsRNA induced IL-8 mRNA expression in cells treated with AE. Conclusions: We found that AE strongly inhibits Th1 biased responses in epithelium as evident by decreased expression of Th1 biased cytokines.