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Scientific Fields
Diseases
Organisms
Applications
Technique

Published in Proceedings of the National Academy of Sciences of the United States of America - 26 Dec 2017

Aymeric L, Donnadieu F, Mulet C, du Merle L, Nigro G, Saffarian A, Bérard M, Poyart C, Robine S, Regnault B, Trieu-Cuot P, Sansonetti PJ, Dramsi S

Link to Pubmed [PMID] – 29279402

Proc. Natl. Acad. Sci. U.S.A. 2018 Jan;115(2):E283-E291

Colonization bysubsp.(SGG) is strongly associated with the occurrence of colorectal cancer (CRC). However, the factors leading to its successful colonization are unknown, and whether SGG influences the oncogenic process or benefits from the tumor-prone environment to prevail remains an open question. Here, we elucidate crucial steps that explain how CRC favors SGG colonization. By using mice genetically prone to CRC, we show that SGG colonization is 1,000-fold higher in tumor-bearing mice than in normal mice. This selective advantage occurs at the expense of resident intestinal enterococci. An SGG-specific locus encoding a bacteriocin (“gallocin”) is shown to kill enterococci in vitro. Importantly, bile acids strongly enhance this bacteriocin activity in vivo, leading to greater SGG colonization. Constitutive activation of the Wnt pathway, one of the earliest signaling alterations in CRC, and the decreased expression of the bile acid apical transporter gene, as an effect of thefounding mutation, may thereby sustain intestinal colonization by SGG. We conclude that CRC-specific conditions promote SGG colonization of the gut by replacing commensal enterococci in their niche.

https://www.ncbi.nlm.nih.gov/pubmed/29279402