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Gut virome profiling identifies an association between temperate phages and colorectal cancer promoted by Helicobacter pylori infection.
Gut Microbes 15:2257291 (2023)
Colorectal cancer (CRC) is one of the most commonly diagnosed cancers worldwide. While a close correlation between chronic Helicobacter pylori infection and CRC has been reported, the role of the virome has been overlooked. Here, we infected Apc-mutant mouse models and C57BL/6 mice with H. pylori and conducted a comprehensive metagenomics analysis of H. pylori-induced changes in lower gastrointestinal tract bacterial and viral communities. We observed an expansion of temperate phages in H. pylori infected Apc +/1638N mice at the early stage of carcinogenesis. Some of the temperate phages were predicted to infect bacteria associated with CRC, including Enterococcus faecalis. We also observed a high prevalence of virulent genes, such as flgJ, cwlJ, and sleB, encoded by temperate phages. In addition, we identified phages associated with pre-onset and onset of H. pylori-promoted carcinogenesis. Through co-occurrence network analysis, we found strong associations between the viral and bacterial communities in infected mice before the onset of carcinogenesis. These findings suggest that the expansion of temperate phages, possibly caused by prophage induction triggered by H. pylori infection, may have contributed to the development of CRC in mice by interacting with the bacterial community.
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Publication type
Article: Journal article
Document type
Scientific Article
Keywords
Auxiliary Metabolic Genes ; Bacteria-phage Interaction ; Colorectal Cancer ; Helicobacter Pylori ; Temperate Bacteriophage; Trimeric Autotransporter; Gastric-cancer; Inflammation; Populations; Adhesin; Gene; Caga
ISSN (print) / ISBN
1949-0976
e-ISSN
1949-0984
Journal
Gut Microbes
Quellenangaben
Volume: 15,
Issue: 2,
Article Number: 2257291
Publisher
Landes Bioscience
Publishing Place
530 Walnut Street, Ste 850, Philadelphia, Pa 19106 Usa
Non-patent literature
Publications
Reviewing status
Peer reviewed
Institute(s)
Institute of Virology (VIRO)
Grants
The authors thank Sophie E. Smith for proofreading the manuscript, the reviewers and the editor for their constructive comments, as well as members of the Deng Lab for technical support.