期刊
CELL HOST & MICROBE
卷 25, 期 2, 页码 285-+出版社
CELL PRESS
DOI: 10.1016/j.chom.2019.01.008
关键词
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资金
- Health Sciences Center Cores at the University of Utah [5-P39-DK034987, 5-P40-OD010995]
- University of North Carolina
- NIH New Innovator Award [DP2GM111099-01]
- NHLBI [R00HL102228-05]
- NIGMS [GM114817]
- NIH R01 grant [DK114252]
- SHINE program at Boehringer Ingelheim
- University of Utah's seed grant program
- NIH innovator award [DP2AT008746-01]
- Edward Mallinckrodt Jr.
- Pew Scholars Program
- NSF CAREER award [IOS-1253278]
- Packard Fellowship in Science and Engineering NIAID K22 [AI95375]
- Burrough's Wellcome Fund
- American Asthma Foundation
Bacteriophages are the most abundant members of the microbiota and have the potential to shape gut bacterial communities. Changes to bacteriophage composition are associated with disease, but how phages impact mammalian health remains unclear. We noted an induction of host immunity when experimentally treating bacterially driven cancer, leading us to test whether bacteriophages alter immune responses. Treating germ-free mice with bacteriophages leads to immune cell expansion in the gut. Lactobacillus, Escherichia, and Bacteroides bacteriophages and phage DNA stimulated IFN-gamma via the nucleotide-sensing receptor TLR9. The resultant immune responses were both phage and bacteria specific. Additionally, increasing bacteriophage levels exacerbated colitis via TLR9 and IFN-gamma. Similarly, ulcerative colitis (UC) patients responsive to fecal microbiota transplantation (FMT) have reduced phages compared to non-responders, and mucosal IFN-gamma positively correlates with bacteriophage levels. Bacteriophages from active UC patients induced more IFN-gamma compared to healthy individuals. Collectively, these results indicate that bacteriophages can alter mucosal immunity to impact mammalian health.
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