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Spatial disturbances in altered mucosal and luminal gut viromes of diet‐induced obese mice
Author(s) -
Kim MinSoo,
Bae JinWoo
Publication year - 2016
Publication title -
environmental microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.954
H-Index - 188
eISSN - 1462-2920
pISSN - 1462-2912
DOI - 10.1111/1462-2920.13182
Subject(s) - human virome , biology , dysbiosis , gut flora , pika , host (biology) , microbial ecology , temperate climate , microbiome , zoology , microbiology and biotechnology , metagenomics , ecology , bacteria , immunology , genetics , gene , national park
Summary Gut microbial biogeography is a key feature of host–microbe relationships. In gut viral ecology, biogeography and responses to dietary intervention remain poorly understood. Here, we conducted a metagenomic study to determine the composition of the mucosal and luminal viromes of the gut and to evaluate the impact of a W estern diet on gut viral ecology. We found that mucosal and luminal viral assemblages comprised predominantly temperate phages. The mucosal virome significantly differed from the luminal virome in low‐fat diet‐fed lean mice, where spatial variation correlated with bacterial microbiota from the mucosa and lumen. The mucosal and luminal viromes of high‐fat, high‐sucrose ‘Western’ diet‐fed obese mice were significantly enriched with temperate phages of the C audovirales order. Interestingly, this community alteration occurred to a greater extent in the mucosa than lumen, leading to loss of spatial differences; however, these changes recovered after switching to a low‐fat diet. Temperate phages enriched in the W estern diet‐induced obese mice were associated with the B acilli , N egativicutes and B acteroidia classes and temperate phages from the B acteroidia class particularly encoded stress and niche‐specific functions advantageous to bacterial host adaptation. This study illustrates a biogeographic view of the gut virome and phage–bacterial host connections under the diet‐induced microbial dysbiosis.