1.Influence of glucuronoxylomannan of Trichosporon asahii on TLR-2,TLR-4 and TLR-6 in THP-1 cells and its mechanisms
Guangyuan DENG ; Yinglun XIAO ; Ling LI ; Weizheng ZHANG
Chinese Journal of Nosocomiology 2025;35(10):1455-1459
OBJECTIVE To explore the influence of glucuronoxylomannan(GXM)of Trichosporon asahii on Toll-like receptor(TLR)-2,TLR-4 and TLR-6 in human myeloid leukemia mononuclear cell(THP-1)and analyze the molecular mechanisms.METHODS The THP-1 cells were randomly divided into the blank control group(without any treatment after the culture of induced and differentiated THP-1 cells for 8 and 24 hours),and the GXM group(with the induced and differentiated THP-1 cell acting by 500 μg/ml of T.asahii GXM for 8 and 24 hours)after being induced differentiation with phorbol 12-myristate 13-acetate(PMA).The expression levels of TLR-2,TLR-4 and TLR-6 messager ribonucleic acid(mRNA)were detected by real-time fluorescent quantitative polymerase chain reaction(RT-qPCR),and the expression level of TLR-2 protein was detected by means of Western Blot(WB).RESULTS The expression levels of TLR-2,TLR-4 and TLR-6 mRNA of the GXM group were 0.65±0.05,0.46±0.03 and 0.51±0.19,respectively,after the THP-1 cells were acted with GXM for 8 hours,lower than those of the blank control group(P<0.05).After being acting with GXM for 24 hours,the expression level of TLR-2 mRNA of the GXM group was 0.83±0.05,lower than that of the blank control group(t=4.927,P=0.039),and there were no significant differences in the expression levels of TLR-4 and TLR-6 mRNA between the GXM group and the blank control group.The expression level of TLR-2 protein of the GXM group was 85.43±0.40 after the THP-1 cells were acted with GXM for 24 hours,lower than that of the blank control group(t=35.415,P<0.001).CONCLUSION The T.asahii may possess the capabilities of escaping from the phagocytosis of white blood cells and monocytes by increasing the release of GXM,which may help a certain number of fungi escape from the killing by the immune system of the host and establish the persistent infection.
2.Influence of glucuronoxylomannan of Trichosporon asahii on TLR-2,TLR-4 and TLR-6 in THP-1 cells and its mechanisms
Guangyuan DENG ; Yinglun XIAO ; Ling LI ; Weizheng ZHANG
Chinese Journal of Nosocomiology 2025;35(10):1455-1459
OBJECTIVE To explore the influence of glucuronoxylomannan(GXM)of Trichosporon asahii on Toll-like receptor(TLR)-2,TLR-4 and TLR-6 in human myeloid leukemia mononuclear cell(THP-1)and analyze the molecular mechanisms.METHODS The THP-1 cells were randomly divided into the blank control group(without any treatment after the culture of induced and differentiated THP-1 cells for 8 and 24 hours),and the GXM group(with the induced and differentiated THP-1 cell acting by 500 μg/ml of T.asahii GXM for 8 and 24 hours)after being induced differentiation with phorbol 12-myristate 13-acetate(PMA).The expression levels of TLR-2,TLR-4 and TLR-6 messager ribonucleic acid(mRNA)were detected by real-time fluorescent quantitative polymerase chain reaction(RT-qPCR),and the expression level of TLR-2 protein was detected by means of Western Blot(WB).RESULTS The expression levels of TLR-2,TLR-4 and TLR-6 mRNA of the GXM group were 0.65±0.05,0.46±0.03 and 0.51±0.19,respectively,after the THP-1 cells were acted with GXM for 8 hours,lower than those of the blank control group(P<0.05).After being acting with GXM for 24 hours,the expression level of TLR-2 mRNA of the GXM group was 0.83±0.05,lower than that of the blank control group(t=4.927,P=0.039),and there were no significant differences in the expression levels of TLR-4 and TLR-6 mRNA between the GXM group and the blank control group.The expression level of TLR-2 protein of the GXM group was 85.43±0.40 after the THP-1 cells were acted with GXM for 24 hours,lower than that of the blank control group(t=35.415,P<0.001).CONCLUSION The T.asahii may possess the capabilities of escaping from the phagocytosis of white blood cells and monocytes by increasing the release of GXM,which may help a certain number of fungi escape from the killing by the immune system of the host and establish the persistent infection.

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