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.

Gut microbiota-derived succinate: Friend or foe in human metabolic diseases?

“…In the context of disease, several studies have revealed a clear association between gut microbiota disturbances, linked for example to antibiotic-induced dysbiosis [63,64], motility disturbances [65] and specially IBD [34,66,67], and succinate accumulation in the gut lumen. More specifically, there is a wealth of evidence, both in mice and humans, demonstrating that IBD causes an increase in fecal succinate, which has been related to disease activity [68][69][70][71]. While the contribution of intestinal damage versus gut microbiota dysbiosis to this increase in succinate is not clear, a metagenomic study of the gut microbiome of patients with IBD reported a significant decrease in the levels of specific succinate-consuming bacterial strains [72].…”

Taraxacum officinale extract ameliorates dextran sodium sulphate‐induced colitis by regulating fatty acid degradation and microbial dysbiosis

“…Herein, a 16S rDNA sequencing showed that S24‐7, adlercreutzia, anaerostipes, enterococcus, enterobacteriaceae and peptostreptococcaceae had a significant difference between TOEH and DSS groups. The enrichment levels of Bacteroidales S24‐7 and adlercreutzia are decreased, but those of enterobacteriaceae are increased in IBD . Anaerostipes can produce butyrate from acetic and lactic acids, which maintains the intestinal barrier and exerts anti‐inflammatory properties .…”

“…The enrichment levels of Bacteroidales S24-7 and adlercreutzia are decreased, but those of enterobacteriaceae are increased in IBD. 52,53 Anaerostipes can produce butyrate from acetic and lactic acids, which maintains the intestinal barrier and exerts anti-inflammatory properties. 54 Increased abundance of peptostreptococcaceae is associated with ulcerative colitis, 55 colorectal cancer F I G U R E 7 Schematic representation of the proposed mechanism of TOE on DSS-induced colitis.…”

Integrated metabolomics and proteomics of symptomatic and early pre-symptomatic states of colitis

“…Butyrate, propionate and acetate higher levels in day 4 of DSS where similar to the levels of these metabolites in healthy IL-10 -/-, again supporting the similarity between the pre-symptomatic states. However, these findings seem to point to a different behavior in murine models compared to the human disease, as, SCFA levels have been reported to not change significantly in fecal samples of DSS-treated mice (Osaka et al, 2017), whereas reduced levels of SCFA in feces of IBD patients have been reported and linked to a shift in the composition and in the metabolic activity of intestinal microbiota, specifically in the reduction in butyrate-producing bacterial groups (De Preter et al, 2015;Marchesi et al, 2007;Bjerrum et al, 2015).…”