AIM： To explore the effects of retinoic acid receptor-γ （RARγ） on innate immune responses against Aspergillus fumigatus （A. fumigatus） in cultured human corneal epithelial cells （HCECs）. METHODS： The HCECs ...AIM： To explore the effects of retinoic acid receptor-γ （RARγ） on innate immune responses against Aspergillus fumigatus （A. fumigatus） in cultured human corneal epithelial cells （HCECs）. METHODS： The HCECs were stimulated with A. fumigatus hyphae for 0, 2, 4, 8, 12 and 16h. RARγ mRNA and protein levels were tested by quantitative real-time polymerase chain reaction （qRT-PCR） and Western blot. Then HCECs were pretreated with or without BMS961 （RARγ agonist, 1 μg/mL）. The mRNA and protein expression of Dectin-1 and the downstream cytokines （TNF-α and IL-6） were determined by qRT-PCR, Western blot and enzyme-linked immunosorbent assay （ELISA）. RESULTS： The expression of RARγ was upregulated after stimulation with A. fumigatus. RARγ mRNA began to rise at 4h and peaked at 8h （P〈0.001）. The protein of RARγ reached to the peak at 16h （P〈0.001）. Pretreated with BMS961 before A. fumigatus hyphae stimulation, expression of Dectin-1, TNF-α and IL-6 decreased dramatically at mRNA and protein levels. CONCLUSION： HCECs can express RARγ and A. fumigatus hyphae infection can increase RARγ expression. BMS961 can inhibit the expression of Dectin-1 and pro-inflammatory cytokines, and play an anti-inflammatory role in innate immune responses against A. fumigatus.展开更多
基金Supported by National Natural Science Foundation of China(No.81470609No.81500695+2 种基金No.81300730)Key Project of Natural Science Foundation of Shandong Province(No.ZR2012HZ001)Youth Natural Science Foundation of Shandong Province(No.ZR2013HQ007)
文摘AIM： To explore the effects of retinoic acid receptor-γ （RARγ） on innate immune responses against Aspergillus fumigatus （A. fumigatus） in cultured human corneal epithelial cells （HCECs）. METHODS： The HCECs were stimulated with A. fumigatus hyphae for 0, 2, 4, 8, 12 and 16h. RARγ mRNA and protein levels were tested by quantitative real-time polymerase chain reaction （qRT-PCR） and Western blot. Then HCECs were pretreated with or without BMS961 （RARγ agonist, 1 μg/mL）. The mRNA and protein expression of Dectin-1 and the downstream cytokines （TNF-α and IL-6） were determined by qRT-PCR, Western blot and enzyme-linked immunosorbent assay （ELISA）. RESULTS： The expression of RARγ was upregulated after stimulation with A. fumigatus. RARγ mRNA began to rise at 4h and peaked at 8h （P〈0.001）. The protein of RARγ reached to the peak at 16h （P〈0.001）. Pretreated with BMS961 before A. fumigatus hyphae stimulation, expression of Dectin-1, TNF-α and IL-6 decreased dramatically at mRNA and protein levels. CONCLUSION： HCECs can express RARγ and A. fumigatus hyphae infection can increase RARγ expression. BMS961 can inhibit the expression of Dectin-1 and pro-inflammatory cytokines, and play an anti-inflammatory role in innate immune responses against A. fumigatus.
