Gut bacteriome in inflammatory bowel disease: An update on recent advances

• Published in: Indian journal of gastroenterology Vol. 43; no. 1; pp. 103 - 111
• Main Authors: Bajaj, Aditya, Markandey, Manasvini, Kedia, Saurabh, Ahuja, Vineet
• Format: Journal Article
• Language: English
• Published: New Delhi Springer India 01.02.2024
• Subjects: Animals; Bacteria; Colitis, Ulcerative; Crohn Disease - microbiology; Dysbiosis - microbiology; Gastroenterology; Genome-Wide Association Study; Hepatology; Inflammatory Bowel Diseases; Medicine; Medicine & Public Health; Mice; Narrative Review; Inflammatory bowel diseases; Gut bacteriome; Core microbiota; Pathobionts
• ISSN: 0254-8860; 0975-0711; 0975-0711
• DOI: 10.1007/s12664-024-01541-1

Inflammatory bowel diseases (IBD) are chronic inflammatory gut disorders, majorly classified as ulcerative colitis and Crohn’s disease. The complex, multifactorial etiopathogenesis of IBD involves genetic predisposition, environmental cues, aberrant mucosal immune response and a disturbed gut microbiota. Epidemiological trends, studies in gnotobiotic mice models and genome-wide association studies, identifying genes involved in microbial handling, together mount evidence in support of the gut microbiota playing a pivotal role in IBD pathogenesis. Both Crohn’s disease and ulcerative colitis are characterized by severe dysbiosis of the gut microbiome, marked by an expansion of detrimental taxa and concomitant depletion of beneficial members. IBD is characterized by reduction in abundances of bacterial genera involved in production of short-chain fatty acids, bio-transformations of bile acids and synthesis of indole-based tryptophan compounds such as Faecalibacterium , Ruminococcus , Coprococcus , Dorea , Parabacteroides , Eubacterium , Oscillibacter and Prevotella and elevation in members of phyla Proteobacteria and Actinobacteria. This imbalance not only results in exaggerated immune signaling towards the microbial antigens, but also results in an altered metabolomic milieu that triggers additional inflammatory cascades. The present review provides insights into the bacterial dysbiosis observed across different intestinal sites and their metabolomic imprints participating in IBD.