論文

2020年5月

Dietary AhR Ligands Regulate AhRR Expression in Intestinal Immune Cells and Intestinal Microbiota Composition

INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
  • Oliver Schanz
  • ,
  • Rieka Chijiiwa
  • ,
  • Sevgi Can Cengiz
  • ,
  • Yasmin Majlesain
  • ,
  • Heike Weighardt
  • ,
  • Haruko Takeyama
  • ,
  • Irmgard Forster

21
9
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.3390/ijms21093189
出版者・発行元
MDPI

A diet rich in vegetables and fruit is generally considered healthy because of a high content of phytochemicals, vitamins, and fiber. The phytochemical indole-3-carbinol (I3C), a derivative of glucobrassicin, is sold as a dietary supplement promising diverse health benefits. I3C metabolites act as ligands of the aryl hydrocarbon receptor (AhR), an important sensor for environmental polyaromatic chemicals. Here, we investigated how dietary AhR ligand supplementation influences AhR target gene expression and intestinal microbiota composition. For this, we used AhR repressor (AhRR)-reporter mice as a tool to study AhR activation in the intestine following dietary I3C-supplementation in comparison with AhR ligand-deprived diets, including a high fat diet. AhRR expression in intestinal immune cells was mainly driven by dietary AhR ligands and was independent of microbial metabolites. A lack of dietary AhR ligands caused enhanced susceptibility to dextran sodium sulfate (DSS)-induced colitis and correlated with the expansion of Enterobacteriaceae, whereas Clostridiales, Muribaculaceae, and Rikenellaceae were strongly reduced. I3C supplementation largely reverted this effect. Comparison of I3C-induced changes in microbiota composition using wild-type (WT), AhRR-deficient, and AhR-deficient mice revealed both AhR-dependent and -independent alterations in the microbiome. Overall, our study demonstrates that dietary AhR ligand supplementation has a profound influence on Ahrr expression in intestinal immune cells as well as microbiota composition.

Web of Science ® 被引用回数 : 25

リンク情報
DOI
https://doi.org/10.3390/ijms21093189
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000535581700160&DestApp=WOS_CPL
ID情報
  • DOI : 10.3390/ijms21093189
  • eISSN : 1422-0067
  • Web of Science ID : WOS:000535581700160

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