GUT MICROBIOTA ALTERATIONS IN INFLAMMATORY BOWEL DISEASE: AN IMMUNOMICROBIAL APPROACH

Abstract

 IBD (inflammatory bowel disease) that encompasses both Crohn's disease and ulcerative colitis is increasingly becoming evident that it is a complex interaction between the gut microbiome and immune system.  The paper has investigated gut microbiota changes in inflammatory bowel disease (IBD) through a systematic approach that includes metagenomic, immunological biomarker, and clinical phenotyping.  The findings showed a severe disequilibrium of microbiota, characterized by a significant reduction of beneficial commensals, including Faecalibacterium prausnitzii and Bifidobacterium longum, and an increase in pro-inflammatory ones, including Escherichia coli (adherent-invasive strains) and Ruminococcus gnavus.  Quantitative sequencing showed a decrease in the abundance of short-chain fatty acid (SCFA)-producing bacteria (45-60 percent) with a dramatic increase in the abundance of pathobionts (p < 0.01).  The immunological analysis showed that there was an elevation of mucosal cytokines, such as IL-6, IL-17, and TNF-a, with a positive relationship with indices of dysbiosis (r = 0.72).  Functional metagenomics also demonstrated that microbial metabolic pathways were not functioning efficiently such as those that produce butyrate and those that decompose tryptophan. These channels were closely connected with the extent of wickedness of the illness.  All of the data indicate that it is not only the ecological balance in the gut that is disrupted by IBD-associated dysbiosis but also the process of mucosal immune activation, which leads to self-perpetuating inflammatory cycle.  These findings highlight the importance of microbiota-immune interactions in the pathophysiology of IBD and also suggest the potential of microbiome-targeted therapy as an adjunctive measure in the regulation of the disease.