TY - JOUR
T1 - OGG1 deficiency alters the intestinal microbiome and increases intestinal inflammation in a mouse model
AU - Simon, Holly
AU - Vartanian, Vladimir
AU - Wong, Melissa H.
AU - Nakabeppu, Yusaku
AU - Sharma, Priyanka
AU - Stephen Lloyd, R.
AU - Sampath, Harini
N1 - Funding Information:
The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. This research was supported by NIH grants R01DK075974 (to RSL), DK100640 (to HS), and U24-DK092993 (to the UC Davis Mouse Metabolic Phenotyping Center). We thank Drs. Pawel Jaruga and Miral Dizdaroglu of the National Institute of Standards and Technology for the measurements of DNA damage. We thank Dr. Jody E. Hooper and Paige Davies of Oregon Health & Science University for technical assistance with histological assessments.
Publisher Copyright:
© 2020 Simon et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
PY - 2020/1/1
Y1 - 2020/1/1
N2 - 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.
AB - 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.
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U2 - 10.1371/journal.pone.0227501
DO - 10.1371/journal.pone.0227501
M3 - Article
C2 - 31935236
AN - SCOPUS:85077906372
SN - 1932-6203
VL - 15
JO - PLoS One
JF - PLoS One
IS - 1
M1 - e0227501
ER -
