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Meta-Analysis of Fecal Microbiota and Metabolites in Experimental Colitic Mice during the Inflammatory and Healing Phases.

Abstract
The imbalance of gut microbiota is known to be associated with inflammatory bowel disease, but it remains unknown whether dysbiosis is a cause or consequence of chronic gut inflammation. In order to investigate the effects of gut inflammation on microbiota and metabolome, the sequential changes in gut microbiota and metabolites from the onset of colitis to the recovery in dextran sulfate sodium-induced colitic mice were characterized by using meta 16S rRNA sequencing and proton nuclear magnetic resonance (¹H-NMR) analysis. Mice in the colitis progression phase showed the transient expansions of two bacterial families including Bacteroidaceae and Enterobacteriaceae and the depletion of major gut commensal bacteria belonging to the uncultured Bacteroidales family S24-7, Rikenellaceae, Lachnospiraceae, and Ruminococcaceae. After the initiation of the recovery, commensal Lactobacillus members promptly predominated in gut while other normally abundant bacteria excluding the Erysipelotrichaceae remained diminished. Furthermore, ¹H-NMR analysis revealed characteristic fluctuations in fecal levels of organic acids (lactate and succinate) associated with the disease states. In conclusion, acute intestinal inflammation is a perturbation factor of gut microbiota but alters the intestinal environments suitable for Lactobacillus members.
AuthorsToshifumi Osaka, Eri Moriyama, Shunichi Arai, Yasuhiro Date, Junji Yagi, Jun Kikuchi, Satoshi Tsuneda
JournalNutrients (Nutrients) Vol. 9 Issue 12 (Dec 06 2017) ISSN: 2072-6643 [Electronic] Switzerland
PMID29211010 (Publication Type: Journal Article, Meta-Analysis)
Chemical References
  • RNA, Ribosomal, 16S
  • Dextran Sulfate
Topics
  • Animals
  • Bacteria (classification, genetics, isolation & purification)
  • Colitis (chemically induced)
  • Dextran Sulfate (toxicity)
  • Feces (microbiology)
  • Gastrointestinal Microbiome
  • Inflammation (chemically induced, therapy)
  • Mice
  • RNA, Ribosomal, 16S (genetics)

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