OGG1 deficiency alters the intestinal microbiome and increases intestinal inflammation in a mouse model
Autoři:
Holly Simon aff001; Vladimir Vartanian aff002; Melissa H. Wong aff003; Yusaku Nakabeppu aff005; Priyanka Sharma aff006; R. Stephen Lloyd aff002; Harini Sampath aff006
Působiště autorů:
Division of Environmental and Biomolecular Systems, Institute of Environmental Health, Oregon Health & Science University, Portland, Oregon, United States of America
aff001; Oregon Institute of Occupational Health Sciences, Oregon Health & Science University, Portland, Oregon, United States of America
aff002; Department of Cell, Developmental and Cancer Biology, Oregon Health & Science University, Portland, Oregon, United States of America
aff003; Knight Cancer Institute, Oregon Health & Science University, Portland, Oregon, United States of America
aff004; Division of Neurofunctional Genomics, Department of Immunobiology and Neuroscience, Medical Institute of Bioregulation, Fukuoka, Kyushu, Japan
aff005; Department of Nutritional Sciences, Rutgers, the State University of New Jersey, New Brunswick, New Jersey, United States of America
aff006; New Jersey Institute for Food, Nutrition, and Health, Rutgers, the State University of New Jersey, New Brunswick, New Jersey, United States of America
aff007; Department of Molecular and Medical Genetics, Oregon Health & Science University, Portland, Oregon, United States of America
aff008
Vyšlo v časopise:
PLoS ONE 15(1)
Kategorie:
Research Article
doi:
https://doi.org/10.1371/journal.pone.0227501
Souhrn
OGG1-deficient (Ogg1-/-) animals display increased propensity to age-induced and diet-induced metabolic diseases, including insulin resistance and fatty liver. Since the intestinal microbiome is increasingly understood to play a role in modulating host metabolic responses, we examined gut microbial composition in Ogg1-/- mice subjected to different nutritional challenges. Interestingly, Ogg1-/- mice had a markedly altered intestinal microbiome under both control-fed and hypercaloric diet conditions. Several microbial species that were increased in Ogg1-/- animals were associated with increased energy harvest, consistent with their propensity to high-fat diet induced weight gain. In addition, several pro-inflammatory microbes were increased in Ogg1-/- mice. Consistent with this observation, Ogg1-/- mice were significantly more sensitive to intestinal inflammation induced by acute exposure to dextran sulfate sodium. Taken together, these data indicate that in addition to their proclivity to obesity and metabolic disease, Ogg1-/- mice are prone to colonic inflammation. Further, these data point to alterations in the intestinal microbiome as potential mediators of the metabolic and intestinal inflammatory response in Ogg1-/- mice.
Klíčová slova:
Body weight – Colon – Diet – Gastrointestinal tract – Inflammation – Inflammatory bowel disease – Microbiome – Mouse models
Zdroje
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