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.
Highlights
Inflammatory bowel disease (IBD), which includes Crohn’s disease and ulcerative colitis, is characterized by chronic and relapsing inflammation of the gut
Microbiome studies in IBD patients have reported the reduction in these Treg-inducing bacterial population including Clostridia clusters IV and XIVa [5,6]. These findings indicate the possibility that dysbiosis-induced changes in gut metabolites are responsible for the pathogenesis of IBD
We demonstrate here characteristic dynamics of commensal bacteria and organic acids associated with disease states
Summary
Inflammatory bowel disease (IBD), which includes Crohn’s disease and ulcerative colitis, is characterized by chronic and relapsing inflammation of the gut. The definite pathogenesis of IBD remains unclear, numerous studies have suggested the genetic and environment factors associated with chronic intestinal inflammation. A recent molecular phylogenetic analysis revealed the imbalanced bacterial composition (dysbiosis) in human IBD patients [5,6,7] and IBD model animals [8,9].
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