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Insight into gut dysbiosis of patients with inflammatory bowel disease and ischemic colitis

The collection of whole microbial communities (bacteria, archaea, fungi, and viruses) together constitutes the gut microbiome. Diet, age, stress, host genetics, and diseases cause increases or decreases in the relative abundance and diversity of bacterial species (dysbiosis). We aimed to investigate...

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Bibliographic Details
Published in:Frontiers in microbiology 2023-05, Vol.14, p.1174832-1174832
Main Authors: Dahal, Ram Hari, Kim, Shukho, Kim, Yu Kyung, Kim, Eun Soo, Kim, Jungmin
Format: Article
Language:English
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Summary:The collection of whole microbial communities (bacteria, archaea, fungi, and viruses) together constitutes the gut microbiome. Diet, age, stress, host genetics, and diseases cause increases or decreases in the relative abundance and diversity of bacterial species (dysbiosis). We aimed to investigate the gut microbial composition at different taxonomic levels of healthy controls (HCs) with active Crohn's disease (CD), ulcerative colitis (UC), and ischemic colitis (IC) using culture- and non-culture-based approaches and identify biomarkers to discriminate CD, UC, or IC. We determined the specific changes in the gut microbial profile using culture-independent (16S rRNA gene amplicon sequencing) as well as culture-based (culturomic) approaches. Biomarkers were validated using quantitative Real-Time PCR (qPCR). In both methods, bacterial diversity and species richness decreased in disease-associated conditions compared with that in HCs. Highly reduced abundance of and sp. and an increased abundance of potentially pathogenic bacteria such as , , and in all CD, UC, or IC conditions were observed. We noted a high abundance of in CD patients; in UC patients; and , , and in IC patients. Highly reduced abundance of in all cases, and increased abundance of and in CD, and in UC, and , , and in IC could be biomarkers for CD, UC, and IC, respectively. These biomarkers may help in IBD (CD or UC) and IC diagnosis.
ISSN:1664-302X
1664-302X
DOI:10.3389/fmicb.2023.1174832