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Updated: May 8, 2026

Microbiota Analysis Using Two-step PCR and Next-generation 16S rRNA Gene Sequencing
Published on: October 15, 2019
Is the microbiome the answer to inflammatory bowel disease: systematic review
Devansh Shah1,2, Fiona Phan3, Zirong Yu4
1Department of Colorectal Surgery, Westmead Hospital, Corner Hawkesbury Road and Darcy Roads, Westmead, NSW, 2145, Australia.
Purpose:
Inflammatory bowel disease (IBD) encompasses two main conditions - Crohn's disease (CD) and ulcerative colitis (UC). Its pathogenesis is vastly unknown but genetics, environmental factors and the gut microbiome are thought to play vital roles. While dysbiosis is thought to be a feature of IBD, its exact role in pathogenesis is unclear.
Methods:
Relevant studies were identified through searching Medline and Embase from database inception to January 2025. Only gastrointestinal microbiome studies comparing IBD human patients with healthy controls (HC), performed on faecal, mucosal biopsy, saliva, or oral swab samples were examined. Studies were excluded if they included ≤ 10 IBD patients, did not compare IBD to HC, reported on IBD with other gastrointestinal infections, all were taking IBD medications, or included post-operative bowel resection patients.
Results:
Of 83 identified observational studies, most reported reduced alpha and beta diversity in IBD, more prevalent in CD than UC. There was depletion of protective butyrate producing Firmicutes bacteria including Faecalibacterium (specifically F. prausnitzii), Eubacteria, Roseburia, Lachnospiraceae, Ruminococcaceae (mainly R. bromii). There was decreased Bacteroidetes phylum in IBD, with depletion of Bacteroides genus in CD but increased in UC. There was increased Proteobacteria and its family Enterobacteriaceae in IBD.
Conclusions:
The gut microbiome in IBD demonstrated reduced biodiversity, more pronounced in CD, with increased pathogenic and reduced beneficial bacteria. While this study demonstrated important associations between the microbiome and IBD, the exact mechanism, whether it be from a multistep process, a causative agent, or interplay between mucosal immunology and dysbiosis, is yet be elucidated.
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