The fungal cell wall component β-glucan activates inflammation via the Dectin-1 receptor and IL-17 coordinates the antifungal immunity. However, the molecular crosstalk between IL-17, Dectin-1, and β-glucan in epithelial cells and fungal immunity remains unclear. We investigated the impact of A.fumigatus-derived β-glucan (AFBG) and C.albicans-derived β-glucan (CABG) on Dectin-1 and cytokines in nasal epithelial cells (NECs) and bronchial epithelial cells (BECs) in the presence of IL-17. CABG reduced BEC viability more than AFBG despite similar Dectin-1 expression. IL-17 reduced β-glucan-dependent Dectin-1 expression in NECs but increased it in BECs after 12 h. AFBG synergized with IL-17, enhancing pro-inflammatory cytokines and chemokine expressions. IL-6 and IL-8 production increased in the presence of IL-17. Th17 cytokine influenced the Dectin-1 response to fungal β-glucan in NECs and BECs, impacting the initiation and nature of epithelial cell reactions to AFBG and CABG. Uncovering the molecular mechanisms of fungal β-glucans in the respiratory tract could lead to novel strategies for preventing fungal diseases.