Intest Res.  2024 Jan;22(1):15-43. 10.5217/ir.2023.00080.

Gut microbiota in pathophysiology, diagnosis, and therapeutics of inflammatory bowel disease

Affiliations
  • 1Redcliffe Labs, Noida, India
  • 2School of Biological Sciences, Nanyang Technological University, Singapore
  • 3Centre for Microbiome Medicine, Lee Kong Chian School of Medicine, Nanyang Technological University, Singapore
  • 4Department of Zoology, Ramjas College, University of Delhi, Delhi, India

Abstract

Inflammatory bowel disease (IBD) is a multifactorial disease, which is thought to be an interplay between genetic, environment, microbiota, and immune-mediated factors. Dysbiosis in the gut microbial composition, caused by antibiotics and diet, is closely related to the initiation and progression of IBD. Differences in gut microbiota composition between IBD patients and healthy individuals have been found, with reduced biodiversity of commensal microbes and colonization of opportunistic microbes in IBD patients. Gut microbiota can, therefore, potentially be used for diagnosing and prognosticating IBD, and predicting its treatment response. Currently, there are no curative therapies for IBD. Microbiota-based interventions, including probiotics, prebiotics, synbiotics, and fecal microbiota transplantation, have been recognized as promising therapeutic strategies. Clinical studies and studies done in animal models have provided sufficient evidence that microbiota-based interventions may improve inflammation, the remission rate, and microscopic aspects of IBD. Further studies are required to better understand the mechanisms of action of such interventions. This will help in enhancing their effectiveness and developing personalized therapies. The present review summarizes the relationship between gut microbiota and IBD immunopathogenesis. It also discusses the use of gut microbiota as a noninvasive biomarker and potential therapeutic option.

Keyword

Inflammatory bowel disease; Ulcerative colitis; Crohn disease; Microbiota; Fecal microbiota transplantation

Figure

  • Fig. 1. Microbes involved in inflammatory bowel disease and their molecular mechanisms. Figure created with BioRender. B. fragilis, Bacteroides fragilis; E. faecium, Enterococcus faecium; E. coli, Escherichia coli; F. nucleatum, Fusobacterium nucleatum; F. prausnitzii, Faecalibacterium prausnitzii; M. stadtmanae, Methanosphaera stadtmanae; R. gnavus, Ruminococcus gnavus; TLR4, Toll-like receptor 4; BFT, B. fragilis toxin; TNF, tumor necrosis factor; ETBF, enterotoxigenic B. fragilis; AhR, aryl hydrocarbon receptor; IL, interleukin; PLC, phospholipase C; DAG, diacylglycerol; PKC, protein kinase C.

  • Fig. 2. Microbial metabolites implicated in inflammatory bowel disease (IBD) and their molecular mechanisms. Figure created with BioRender. SCFA, short-chain fatty acid; PXR, pregnane X receptor; AhR, aryl hydrocarbon receptor; IL, interleukin; Treg, T regulatory; GPCRs, G protein-coupled receptors; CD, Crohn’s disease; UC, ulcerative colitis; FXR, farnesoid X receptor; TGR5, transmembrane G protein-coupled receptor 5.


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