THE HUMAN GUT REPRESENTS ONE of the most diverse bacterial ecosystems. These bacteria live in a mutualistic state with the host; however, when this homeostatic balance is perturbed by an alteration in bacterial community composition and function (dysbiosis), it can lead to disruption of normal host physiology. A role for gut microbiota has been suggested in pathogenesis of colorectal cancer based on recent mouse and human studies. In a mouse model of colitis-associated colorectal cancer, Uronis et al. (24) found that risk for tumorigenesis was lower in germ-free conditions than with a conventional microbiome. In another study Kostic et al. (11) found that Fusobacterium species were enriched in colorectal cancer patients. They attributed this enrichment to the strong adhesive and invasive abilities of Fusobacterium for epithelial cells, which allows them to take up residence in tumor environment. Kostic et al. also showed that introduction of Fusobacterium species in the Apc Min/ mouse model, a genetic mouse model of colon cancer, accelerates colonic tumorigenesis (11). These studies support a role for gut microbiota in the pathogenesis of colorectal cancer, but there is little known about factors that promote dysbiosis leading to colorectal cancer and how preventing dysbiosis might be protective. The present study by Higashimura et al. (10a) helps answer this question by investigating effects of high-fat diet (HFD) on gut microbiota and host function and supplementing HFD with a prebiotic to prevent changes in gut microbiota.
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Bhattarai et al. (2016) studied this question.
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