Alteration of the Gut Microbiome in Inflammatory Bowel Disease

Abstract

<b><i>Background:</i></b> Alteration of the gut microbial structure and function (dysbiosis) is associated with the pathogenesis of various disorders including inflammatory bowel disease (IBD). <b><i>Summary:</i></b> Under normal conditions, β-oxidation of butyrate consumes oxygen in colonocytes and maintains the anaerobic environment in the lumen. Depletion of butyrate-producing bacteria results in anaerobic glycolysis in colonocytes and increases oxygen diffusion into the lumen, leading to a luminal facultative anaerobe expansion. Dysbiosis in IBD is characterized by the reduced abundance of the phylum Firmicutes (e.g., <i>Faecalibacterium</i>, <i>Roseburia</i>, and <i>Ruminococcus</i>) and an increase of the phylum Proteobacteria (e.g., <i>Enterobacteriaceae</i>). The overall structure of the gut mycobiome differs markedly in IBD patients, particularly Crohn’s disease (CD), compared with healthy individuals. An increase in the genus <i>Candida</i> is a major contributory factor in the alteration of the mycobiome in Japanese CD patients, but an increase in the genus <i>Saccharomyces</i> is characteristic in Western patients. The gut virome, which is mainly composed of bacteriophages (phages), influences gut homeostasis and pathogenic conditions via an interaction with the gut bacterial community. Alterations in the gut virome have been suggested in patients with IBD. This may alter either the immunogenicity of bacteria, thus affecting the bacteria-host interactions, or the bacterial functions such as antibiotic resistance and toxin synthesis. <b><i>Key Message:</i></b> Advances in DNA sequencing technology and bioinformatics have revolutionized our understanding of the microbiome in the gut.