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The inflammation regulation effects of Enterococcus faecium HDRsEf1 on human enterocyte-like HT-29 cells

Animal Cells and Systems 2016년 20권 2호 p.70 ~ 76
Tian Zhongyuan, Yang Lu, Li Penghui, Xiao Yuncai, Peng Jian, Wang Xiliang, Li Zili, Liu Mei, Bi Dingren, Shi Deshi,
소속 상세정보
 ( Tian Zhongyuan ) - Huazhong Agricultural University College of Veterinary Medicine
 ( Yang Lu ) - Huazhong Agricultural University College of Veterinary Medicine
 ( Li Penghui ) - Huazhong Agricultural University College of Veterinary Medicine
 ( Xiao Yuncai ) - Huazhong Agricultural University College of Veterinary Medicine
 ( Peng Jian ) - Huazhong Agricultural University College of Animal Science and Technology Department of Animal Nutrition and Feed Science
 ( Wang Xiliang ) - Huazhong Agricultural University College of Veterinary Medicine
 ( Li Zili ) - Huazhong Agricultural University College of Veterinary Medicine
 ( Liu Mei ) - Huazhong Agricultural University College of Veterinary Medicine
 ( Bi Dingren ) - Huazhong Agricultural University College of Veterinary Medicine
 ( Shi Deshi ) - Huazhong Agricultural University College of Veterinary Medicine

Abstract


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-1β, IL-6, IL-8, IL-12p35, IL-17, and TNF-α and did not affect the anti-inflammatory factors IL-10, PPAR-γ, and TSLP; besides HDRsEf1 did not upregulate the degradation of IκB in HT-29 cells. By contrast, enterohemorrhagic E. coli (EHEC) O157:H7 strongly up-regulated the mRNA level of pro-inflammatory factors IL-1β, IL-6, IL-8, IL-23, and TNF-α, downregulated obviously anti-inflammatory factor PPAR-?, and obviously upregulated the degradation of IκB, 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.

키워드

Enterococcus faecium HDRsEf1; HT-29 cells; NF-κb/IκB; toll-like receptor

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