期刊
SCIENTIFIC REPORTS
卷 8, 期 -, 页码 -出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/s41598-018-26763-0
关键词
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资金
- National Research Foundation - Ministry of Science and ICT [NRF-2015R1D1A1A02061577, NRF-2018R1A2B2006793]
- SNU-Yonsei Research Cooperation Program through Seoul National University
- Cooperative Research Program for Agriculture Science and Technology Development, Rural Development Administration, Republic of Korea [PJ01336401]
The gut microbiota in chicken has long been studied, mostly from the perspective of growth performance. However, there are some immunological studies regarding gut homeostasis in chicken. Although CD4(+)CD25(+)T cells are reported to act as regulatory T cells (Tregs) in chicken, there have been no studies showing the relationship between gut microbiota and Tregs. Therefore, we established a model for 'antibiotics (ABX)-treated chickens' through administration of an antibiotic cocktail consisting of ampicillin, gentamycin, neomycin, metronidazole, and vancomycin in water for 7 days. CD4(+)CD8(-)CD25(+) and CD4(+)CD8(+)CD25(+)T cells in cecal tonsils were significantly decreased in this model. Gram-positive bacteria, especially Clostridia, was responsible for the changes in CD4(+)CD8(-)CD25(+) or CD4(+)CD8(+)CD25(+)T cells in cecal tonsils. Feeding ABX-treated chickens with acetate recovered CD4(+)CD8(-)CD25(+) and CD4(+)CD8(+)CD25(+)T cells in cecal tonsils. GPR43, a receptor for acetate, was highly expressed in CD4(+)CD8(-)CD25(+)T cells. In conclusion, our study demonstrated that the gut microbiota can regulate the population of CD4+CD- CD2(5)+ and CD4(+)CD8(+)CD25(+)T cells, and that acetate is responsible for the induction of CD4+CD- CD2(5)+T cells in cecal tonsils via GPR43.
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