<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Gutierrez-Orozco F</submitter><funding>NIDCR NIH HHS</funding><funding>NCI NIH HHS</funding><pagination>1226-38</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC4076011</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>58(6)</volume><pubmed_abstract>Ulcerative colitis (UC) is a chronic inflammatory disease of the colon. ?-Mangostin (?-MG), the most abundant xanthone in mangosteen fruit, exerts anti-inflammatory and antibacterial activities in vitro. We evaluated the impact of dietary ?-MG on murine experimental colitis and on the gut microbiota of healthy mice.Colitis was induced in C57BL/6J mice by administration of dextran sulfate sodium (DSS). Mice were fed control diet or diet with ?-MG (0.1%). ?-MG exacerbated the pathology of DSS-induced colitis. Mice fed diet with ?-MG had greater colonic inflammation and injury, as well as greater infiltration of CD3(+) and F4/80(+) cells, and colonic myeloperoxidase, than controls. Serum levels of granulocyte colony-stimulating factor, IL-6, and serum amyloid A were also greater in ?-MG-fed animals than in controls. The colonic and cecal microbiota of healthy mice fed ?-MG but no DSS shifted to an increased abundance of Proteobacteria and decreased abundance of Firmicutes and Bacteroidetes, a profile similar to that found in human UC.?-MG exacerbated colonic pathology during DSS-induced colitis. These effects may be associated with an induction of intestinal dysbiosis by ?-MG. Our results suggest that the use of ?-MG-containing supplements by patients with UC may have unintentional risk.</pubmed_abstract><journal>Molecular nutrition &amp; food research</journal><pubmed_title>Dietary ?-mangostin, a xanthone from mangosteen fruit, exacerbates experimental colitis and promotes dysbiosis in mice.</pubmed_title><pmcid>PMC4076011</pmcid><funding_grant_id>P30 CA016058</funding_grant_id><funding_grant_id>T32 DE014320</funding_grant_id><pubmed_authors>Mace T</pubmed_authors><pubmed_authors>Berman-Booty LD</pubmed_authors><pubmed_authors>Clinton SK</pubmed_authors><pubmed_authors>Galley JD</pubmed_authors><pubmed_authors>Bailey MT</pubmed_authors><pubmed_authors>Suksamrarn S</pubmed_authors><pubmed_authors>Chitchumroonchokchai C</pubmed_authors><pubmed_authors>Failla ML</pubmed_authors><pubmed_authors>Thomas-Ahner JM</pubmed_authors><pubmed_authors>Gutierrez-Orozco F</pubmed_authors><pubmed_authors>Lesinski GB</pubmed_authors></additional><is_claimable>false</is_claimable><name>Dietary ?-mangostin, a xanthone from mangosteen fruit, exacerbates experimental colitis and promotes dysbiosis in mice.</name><description>Ulcerative colitis (UC) is a chronic inflammatory disease of the colon. ?-Mangostin (?-MG), the most abundant xanthone in mangosteen fruit, exerts anti-inflammatory and antibacterial activities in vitro. We evaluated the impact of dietary ?-MG on murine experimental colitis and on the gut microbiota of healthy mice.Colitis was induced in C57BL/6J mice by administration of dextran sulfate sodium (DSS). Mice were fed control diet or diet with ?-MG (0.1%). ?-MG exacerbated the pathology of DSS-induced colitis. Mice fed diet with ?-MG had greater colonic inflammation and injury, as well as greater infiltration of CD3(+) and F4/80(+) cells, and colonic myeloperoxidase, than controls. Serum levels of granulocyte colony-stimulating factor, IL-6, and serum amyloid A were also greater in ?-MG-fed animals than in controls. The colonic and cecal microbiota of healthy mice fed ?-MG but no DSS shifted to an increased abundance of Proteobacteria and decreased abundance of Firmicutes and Bacteroidetes, a profile similar to that found in human UC.?-MG exacerbated colonic pathology during DSS-induced colitis. These effects may be associated with an induction of intestinal dysbiosis by ?-MG. Our results suggest that the use of ?-MG-containing supplements by patients with UC may have unintentional risk.</description><dates><release>2014-01-01T00:00:00Z</release><publication>2014 Jun</publication><modification>2020-10-29T13:38:29Z</modification><creation>2019-03-27T01:31:04Z</creation></dates><accession>S-EPMC4076011</accession><cross_references><pubmed>24668769</pubmed><doi>10.1002/mnfr.201300771</doi></cross_references></HashMap>