期刊
SCIENCE
卷 370, 期 6516, 页码 549-+出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.aay9097
关键词
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资金
- NIAID [U19-A1067798, R35-CA232109, T32-CA009156]
- NMSS [CA10068, P01-DK094779]
- NIH [P40-OD010995, P30-DK34987, P30-DK056350]
- Crohn's and Colitis Foundation
- [Center for Gastrointestinal Biology and Disease (CGIBD)]
- NCI Center Core Support Grant [CA16086]
- UNC Center for Environmental Health and Susceptibility
- NIEHS [ES024950, P30-ES010126]
- Duke Adult Blood and Marrow Transplant Program [R21AG066388]
- ASH Scholar Award
- Memorial Sloan Kettering Cancer Center [K08HL143189, NCI P30 CA008748, R01-CA228358, R01-CA228308, R01-HL147584, P30 CA008748, P01CA023766, P01-AG052359, U01 AI124275, UC6-AI058607]
Ionizing radiation causes acute radiation syndrome, which leads to hematopoietic, gastrointestinal, and cerebrovascular injuries. We investigated a population of mice that recovered from high-dose radiation to live normal life spans. These elite-survivors harbored distinct gut microbiota that developed after radiation and protected against radiation-induced damage and death in both germ-free and conventionally housed recipients. Elevated abundances of members of the bacterial taxa Lachnospiraceae and Enterococcaceae were associated with postradiation restoration of hematopoiesis and gastrointestinal repair. These bacteria were also found to be more abundant in leukemia patients undergoing radiotherapy, who also displayed milder gastrointestinal dysfunction. In our study in mice, metabolomics revealed increased fecal concentrations of microbially derived propionate and tryptophan metabolites in elite-survivors. The administration of these metabolites caused long-term radioprotection, mitigation of hematopoietic and gastrointestinal syndromes, and a reduction in proinflammatory responses.
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