new perspective of human body unravels an Aecosystem that is established by a symbiotic relationship between the gut microbiota and the host. This interaction contributes to maintaining homeostasis in the… Click to show full abstract
new perspective of human body unravels an Aecosystem that is established by a symbiotic relationship between the gut microbiota and the host. This interaction contributes to maintaining homeostasis in the host and provides a nutrient-rich environment for the microbiota. The aberrant microbial composition and metabolic activity of the gut microbiome has been implicated as risk factors or a consequences of several diseases in humans, such as inflammatory bowel disease (IBD) and colorectal cancer. Therefore, precision modification of the gut microbiota is a potential approach for maintaining human health and for disease prevention and treatment. There has been a growing interest in identification of the impact of vitamin D deficiency on carcinogenesis in cancer research. Vitamin D exerts its biologic functions through binding to the nuclear receptor, vitamin D receptor (VDR). Results from a large cohort suggest that higher level of VDR expression is associated with longer survival after surgical resection in patients with colorectal cancer. This clinical evidence is supported by studies from Zhang et al to elucidate a previously unrecognized mechanism through which the intestinal epithelial VDR regulates the homeostasis of the gut microbiome for preventing development of inflammation-associated colorectal cancer. Through a series of elegant in vivo and in vitro studies using human samples and mouse models of colorectal cancer, they report that the absence of VDR in intestinal epithelial cells results in shifting the gut bacterial profile toward that with high risk for colorectal cancer. They further demonstrate that dysbiosis in mice with VDR deletion in intestinal epithelial cells promotes tumorigenesis through stimulating antiinflammatory JAK/STAT3 signaling in intestinal epithelial cells. It has been reported that alterations in the composition, distribution, or metabolism of the gut microbiota may produce an environment in the colon that promotes inflammation, dysplasia, and cancer. Studies from Sun’s group provide an encouraging base from which to further seek host factors that contribute to regulate the symbiotic relationship between gut microbial community and the host for maintaining intestinal homeostasis and protecting against diseases. Although findings from previous studies have revealed that host genetics and environmental factors, such as diet, nutrient availability, immunologic responses, and disease states, shape the composition of the gut microbiota, knowledge about how the host reinforces the microbial communities is not understood. Intestinal epithelial cells localizing on the mucosal surface exert front line responses
               
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