期刊
CELL REPORTS
卷 10, 期 11, 页码 1861-1871出版社
CELL PRESS
DOI: 10.1016/j.celrep.2015.02.049
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资金
- Howard Hughes Medical Institute (International Early Career Scientist
- HHMI) [55007436]
- Fundacao para a Ciencia e Tecnologia [PTDC/BIA-EVF/118075/2010, RECI/IMI-IMU/0038/2012]
- Ministerio de Ciencia e Innovacion (MICINN) [SAF2011-29458]
- Marie-Curie Career Integration Grant [PCIG09-GA-2011-293894]
- Fundação para a Ciência e a Tecnologia [RECI/IMI-IMU/0038/2012, PTDC/BIA-EVF/118075/2010] Funding Source: FCT
The mammalian gut microbiota harbors a diverse ecosystem where hundreds of bacterial species interact with each other and their host. Given that bacteria use signals to communicate and regulate group behaviors (quorum sensing), we asked whether such communication between different commensal species can influence the interactions occurring in this environment. We engineered the enteric bacterium, Escherichia coli, to manipulate the levels of the interspecies quorum sensing signal, autoinducer-2 (AI-2), in the mouse intestine and investigated the effect upon antibiotic-induced gut microbiota dysbiosis. Escherichia coli that increased intestinal AI-2 levels altered the composition of the antibiotic-treated gut microbiota, favoring the expansion of the Firmicutes phylum. This significantly increased the Firmicutes/Bacteroidetes ratio, to oppose the strong effect of the antibiotic, which had almost cleared the Firmicutes. This demonstrates that AI-2 levels influence the abundance of the major phyla of the gut microbiota, the balance of which is known to influence human health.
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