KMID : 1161520160200020070
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Animal Cells and Systems 2016 Volume.20 No. 2 p.70 ~ p.76
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The inflammation regulation effects of Enterococcus faecium HDRsEf1 on human enterocyte-like HT-29 cells
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Tian Zhongyuan
Yang Lu Li Penghui Xiao Yuncai Peng Jian Wang Xiliang Li Zili Liu Mei Bi Dingren Shi Deshi
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Abstract
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Enterococcus faecium HDRsEf1 strain used as a probiotic to inhibit intestine inflammation and improve animal growth performance has been proved by our research team; however, it remains unclear how HDRsEf1 was recognized by intestine cells and how it activates the downstream pathway which benefit intestine health. In this study, HDRsEf1 was used to stimulate HT-29 cell line to partially uncover the intestine benefit mechanism of HDRsEf1. The results of cell viability assays showed that HDRsEf1 had no toxicity on HT-29 at concentrations up to 1?¡¿?108 CFU/mL, HDRsEf1 could upregulate the TLR1, TLR2, and TLR6 mRNA level, especially TLR2, and significantly downregulate the mRNA level of TLR4, TLR5, TLR7, TLR8, but did not significantly affect the mRNA or protein level of MyD88, which suggests that HDRsEf1 activates the TLR2 pathway in an MyD88-independent pattern. HDRsEf1 could significantly downregulate the mRNA level of pro-inflammatory factors IL-1¥â, IL-6, IL-8, IL-12p35, IL-17, and TNF-¥á and did not affect the anti-inflammatory factors IL-10, PPAR-¥ã, and TSLP; besides HDRsEf1 did not upregulate the degradation of I¥êB in HT-29 cells. By contrast, enterohemorrhagic E. coli (EHEC) O157:H7 strongly up-regulated the mRNA level of pro-inflammatory factors IL-1¥â, IL-6, IL-8, IL-23, and TNF-¥á, downregulated obviously anti-inflammatory factor PPAR-?, and obviously upregulated the degradation of I¥êB, which suggested that HDRsEf1 may act as an antagonist to regulate intestine inflammation response to intestine pathogen. These findings shed a light on the intestine benefit mechanism of HDRsEf1.
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KEYWORD
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Enterococcus faecium HDRsEf1, HT-29 cells, NF-¥êb/I¥êB, toll-like receptor
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