期刊
JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
卷 68, 期 10, 页码 3112-3120出版社
AMER CHEMICAL SOC
DOI: 10.1021/acs.jafc.9b07701
关键词
butyrate; antibiotic; gestation and nursing; IFN-gamma(+) T cells; type 1 diabetes; pancreatic immune disorder
资金
- National Natural Science Foundation of China [81870439, 81901670, 81973322, 91642114, 31570915, 81573420]
- National Natural Science Foundation of China (National Youth 1000 Talents Plan)
- Jiangsu Province Recruitment Plan for High-level, Innovative and Entrepreneurial Talents (Innovative Research Team)
- Jiangsu Province Six Summit Talents program [2019-YY-038]
- collaborative innovation center of food safety and quality control in Jiangsu Province
- National FirstClass Discipline Program of Food Science and Technology [JUFSTR20180103]
- Wuxi Social Development Funds for International Science & Technology Cooperation [WX0303B010518180007PB]
- Chinese Postdoctoral Science Foundation [2018M642169]
- Jiangsu Postdoctoral Research Foundation [2018K237C]
- Jiangsu Province Qing Lan Project
Maternal gut dysbiosis affects the development of the offspring immune system. Our previous study has indicated that microbial metabolite butyrate directly shapes pancreatic immune tolerance and dampens type 1 diabetes (T1D) progression. Therefore, maternal butyrate intervention may protect their offspring from maternal gut dysbiosis-accelerated T1D. To test this, pregnant nonobese diabetic (NOD) mice were treated with vancomycin in drinking water with or without a butyrate-supplemented diet during gestation and nursing (oral vancomycin is used to induce maternal gut dysbiosis). Three weeks after delivery, T1D-associated innate and adaptive immune cells were detected to investigate the effects of butyrate on the vancomycin-exacerbated pancreatic immune disorder in dams and pups. The results showed that butyrate inhibited maternal vancomycin-exacerbated secretion of proinflammation cytokines (interferon gamma and interleukin-1 beta) and maternal vancomycin-exacerbated recruitment of interferon gamma(+) T cells (cytotoxic T lymphocytes 1 cells and T helper type 1 cells) in the pancreas of the female offspring, thus dampening T1D development. The protection may be due to butyrate inhibiting the activation of pancreatic dendritic cells (DCs). Our data thus demonstrate that maternal gut dysbiosis can exacerbate pancreatic-directed autoimmunity in the female offspring through T cell- and DC-associated mechanisms that are inhibited by butyrate.
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