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Review
. 2024 Mar 5;44(1):11.
doi: 10.1186/s41232-024-00321-w.

Metabolic network of the gut microbiota in inflammatory bowel disease

Kohei Sugihara  1 , Nobuhiko Kamada  2   3   4
Affiliations
Review

Metabolic network of the gut microbiota in inflammatory bowel disease

Kohei Sugihara et al. Inflamm Regen. .

Abstract

Gut dysbiosis is closely linked to the pathogenesis of inflammatory bowel disease (IBD). Emerging studies highlight the relationship between host metabolism and the modulation of gut microbiota composition through regulating the luminal microenvironment. In IBD, various disease-associated factors contribute to the significant perturbation of host metabolism. Such disturbance catalyzes the selective proliferation of specific microbial populations, particularly pathobionts such as adherent invasive Escherichia coli and oral-derived bacteria. Pathobionts employ various strategies to adapt better to the disease-associated luminal environments. In addition to the host-microbe interaction, recent studies demonstrate that the metabolic network between commensal symbionts and pathobionts facilitates the expansion of pathobionts in the inflamed gut. Understanding the metabolic network among the host, commensal symbionts, and pathobionts provides new insights into the pathogenesis of IBD and novel avenues for treating IBD.

Keywords: AIEC; Gut microbiota; IBD; Metabolic network; Pathobiont.

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Conflict of interest statement

The authors declare that they have no competing interests.

Figures

Fig. 1
Fig. 1
The mechanisms of gut inflammation caused by colonization of IBD-associated pathobionts. AIEC can adhere to and invade the epithelial cells, impairing the epithelial barrier. After invasion to the host, AIEC triggers IL-1β secretion from mononuclear phagocytes, such as macrophages, promoting the differentiation to Th17 cells. Oral pathobionts, including K. pneumoniae and K. aerogenes, can ectopically colonize the gut during gut inflammation. Ectopic colonization of oral pathobionts promotes the production of proinflammatory cytokines from DCs and macrophages, which facilitate the differentiation into Th1 and Th17 cells. Mucolytic bacteria, such as R. gnavus, may promote the encroachment of other bacteria to the epithelial niche. R. gnavus also produces the polysaccharide that promotes tumor necrosis factor (TNF) secretion from DCs
Fig. 2
Fig. 2
The role of host-microbe interaction in expanding pathobionts and pathogens during gut inflammation. Gut inflammation changes the host epithelial metabolism, which provides nutrients and electron acceptors for the expansion of pathobionts and pathogens. Pathobionts and pathogens also utilize unique mucosal nutrients, such as ethanolamine and propanediol, that commensals cannot use for growth. In the inflamed gut, AIEC up-regulates L-serine metabolism and operates diet-derived L-serine for competitive fitness with commensal E. coli
Fig. 3
Fig. 3
Direct and indirect metabolic interaction between commensals, pathobionts, and pathogens. Commensal Bacteroides spp. provide succinate and host-mucus derived sialic acids and fucose for the expansion of pathogenic bacteria, including EHEC, C. difficile, S. Typhimurium, and commensal E. coli (Direct metabolic network). Mucolytic bacteria, such as A. muciniphila, degrade intestinal mucus, promoting the encroachment of AIEC to the intestinal epithelium. In the epithelial niche, AIEC liberates host-derived L-serine for expansion under L-serine deficient conditions (Indirect metabolic network)
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