論文

国際誌
2022年2月

Impact of dietary fructooligosaccharides (FOS) on murine gut microbiota and intestinal IgA secretion.

3 Biotech
  • Aditi Jangid
  • ,
  • Shinji Fukuda
  • ,
  • Tamotsu Kato
  • ,
  • Masahide Seki
  • ,
  • Yutaka Suzuki
  • ,
  • Todd D Taylor
  • ,
  • Hiroshi Ohno
  • ,
  • Tulika Prakash

12
2
開始ページ
56
終了ページ
56
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1007/s13205-022-03116-3

Fructooligosaccharides (FOS) are considered as prebiotics and are well known for their health-promoting properties, including antitumor, allergy-preventive, and infection-protective effects. They exert these effects by modulating the gut microbial composition and dynamics. In the present study, we performed a comparative whole metagenome shotgun sequencing analysis (WMGS) to elucidate the gut microbiota and secretary Immunoglobulin A (SIgA) dynamics as a result of 5% (w/w) FOS supplementation over a period of 7 days (fecal samples were collected every day). A number of taxa including Bacteroides, Lactobacillus, Roseburia, Clostridia, Faecalibaculum, and Enterorhabdus were found to be modulated with SIgA production in the murine gut. The process of SIgA production from FOS metabolization was found to be carried out via the production of short-chain fatty acids in the gut. Species of Bacteroides and Roseburia; namely, B. caccae, B. finegoldii, B. ovatus, B. thetaiotamicron, and Roseburia intestinalis, respectively, are predominantly responsible for FOS metabolization in the murine gut. The abundances of these bacterial species and their corresponding functions involved in FOS metabolization decreased over time even though these prebiotics were administered continuously for seven days. This suggests that there is a decrease in FOS metabolization over time. In addition, the present analysis suggests that the administration of FOS may help to reduce the pathogenic bacteria from the gut via SIgA production. Supplementary Information: The online version contains supplementary material available at 10.1007/s13205-022-03116-3.

リンク情報
DOI
https://doi.org/10.1007/s13205-022-03116-3
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/35186653
PubMed Central
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8811108
ID情報
  • DOI : 10.1007/s13205-022-03116-3
  • PubMed ID : 35186653
  • PubMed Central 記事ID : PMC8811108

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