期刊
SCIENCE
卷 365, 期 6451, 页码 340-+出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.aat9351
关键词
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资金
- NIH New Innovator Award [DP2GM111099-01]
- NHLBI [R00HL102228-05]
- American Cancer Society Research Grant
- Kimmel Scholar Award
- NIGMRS RO1 grant [GM114817]
- Pews Scholar Program
- NIH [R56AI107090]
- Edward Mallinckrodt Jr. Foundation
- NSF CAREER award [IOS-1253278]
- Packard Fellowship in Science and Engineering
- NIAID K22 [AI95375]
- Burroughs Wellcome Investigator in Pathogenesis Award
- American Asthma Foundation
- Margolis Foundation
- MS Society Center grant
- Crohn's and Colitis Foundation Senior Research Award
- [5-P39-DK034987]
- [5-P40-OD010995]
- [R01AG047956]
The microbiota influences obesity, yet organisms that protect from disease remain unknown. During studies interrogating host-microbiota interactions, we observed the development of age-associated metabolic syndrome (MetS). Expansion of Desulfovibrio and loss of Clostridia were key features associated with obesity in this model and are present in humans with MetS. T cell-dependent events were required to prevent disease, and replacement of Clostridia rescued obesity. Inappropriate immunoglobulin A targeting of Clostridia and increased Desulfovibrio antagonized the colonization of beneficial Clostridia. Transcriptional and metabolic analysis revealed enhanced lipid absorption in the obese host. Colonization of germ-free mice with Clostridia, but not Desulfovibrio, down-regulated genes that control lipid absorption and reduced adiposity. Thus, immune control of the microbiota maintains beneficial microbial populations that constrain lipid metabolism to prevent MetS.
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