Summary of study ST001219

This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench, https://www.metabolomicsworkbench.org, where it has been assigned Project ID PR000818. The data can be accessed directly via it's Project DOI: 10.21228/M8Z68P This work is supported by NIH grant, U2C- DK119886.

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Study IDST001219
Study TitleVitamin D regulates the microbiota to induce RORgt/FoxP3+ regulatory T cells
Study SummaryThe active form of vitamin D (1,25(OH)2D) suppresses experimental models of inflammatory bowel disease in part by regulating the microbiota. In this study, the role of vitamin D in the regulation of microbe induced RORgt/FoxP3+ T regulatory (reg) cells in the colon was determined. Vitamin D sufficient (D+) mice had significantly higher frequencies of FoxP3+ and RORgt/FoxP3+ T reg cells in the colon compared to vitamin D deficient (D-) mice. The higher frequency of RORgt/FoxP3+ T reg cells in D+ colon correlated with higher numbers of bacteria from the Clostridium XIVa and Bacteroides in D+ compared to D- cecum. D- mice with fewer RORgt/FoxP3+ T reg cells were significantly more susceptible to colitis than D+ mice. Transfer of the cecal bacteria from D+ or D- mice to germfree recipients phenocopied the higher numbers of RORgt/FoxP3+ cells and reduced susceptibility to colitis in D+ versus D- recipient mice. 1,25(OH)2D treatment of the D- mice beginning at 3 weeks of age did not completely recover RORgt/FoxP3+ T reg cells or the Bacteriodes, Bacteriodes thetaiotaomicron, and Clostridium XIVa numbers to D+ values. Early vitamin D status shapes the microbiota to optimize the population of colonic RORgt/FoxP3+ T reg cells important for resistance to colitis.
Institute
Pennsylvania State University
Last NameNichols
First NameRobert
Address917 Old Boalsburg Road, State College, Pennsylvania, 16801, USA
Emailrgn5011@psu.edu
Phone7247662694
Submit Date2019-07-17
Raw Data AvailableYes
Raw Data File Type(s)pdata, .par, .temp, .fid,.scon2, etc
Analysis Type DetailNMR
Release Date2019-09-23
Release Version1
Robert Nichols Robert Nichols
https://dx.doi.org/10.21228/M8Z68P
ftp://www.metabolomicsworkbench.org/Studies/ application/zip

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Project:

Project ID:PR000818
Project DOI:doi: 10.21228/M8Z68P
Project Title:Vitamin D regulates the microbiota to induce RORgt/FoxP3+ regulatory T cells
Project Summary:The active form of vitamin D (1,25(OH)2D) suppresses experimental models of inflammatory bowel disease in part by regulating the microbiota. In this study, the role of vitamin D in the regulation of microbe induced RORgt/FoxP3+ T regulatory (reg) cells in the colon was determined. Vitamin D sufficient (D+) mice had significantly higher frequencies of FoxP3+ and RORgt/FoxP3+ T reg cells in the colon compared to vitamin D deficient (D-) mice. The higher frequency of RORgt/FoxP3+ T reg cells in D+ colon correlated with higher numbers of bacteria from the Clostridium XIVa and Bacteroides in D+ compared to D- cecum. D- mice with fewer RORgt/FoxP3+ T reg cells were significantly more susceptible to colitis than D+ mice. Transfer of the cecal bacteria from D+ or D- mice to germfree recipients phenocopied the higher numbers of RORgt/FoxP3+ cells and reduced susceptibility to colitis in D+ versus D- recipient mice. 1,25(OH)2D treatment of the D- mice beginning at 3 weeks of age did not completely recover RORgt/FoxP3+ T reg cells or the Bacteriodes, Bacteriodes thetaiotaomicron, and Clostridium XIVa numbers to D+ values. Early vitamin D status shapes the microbiota to optimize the population of colonic RORgt/FoxP3+ T reg cells important for resistance to colitis.
Institute:Pennsylvania State University
Last Name:Nichols
First Name:Robert
Address:650 toftrees Ave apt 108, state college, PA, 16803
Email:rgn5011@psu.edu
Phone:7247662694
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