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Role of the gut microbiota in inflammatory bowel disease pathogenesis: What have we learnt in the past 10 years?
Open accessAbstract
Our understanding of the microbial involvement in inflammatory bowel disease (IBD) pathogenesis has increased exponentially over the past decade. The development of newer molecular tools for the global assessment of the gut microbiome and the identification of nucleotide-binding oligomerization domain-containing protein 2 in 2001 and other susceptibility genes for Crohn's disease in particular has led to better understanding of the aetiopathogenesis of IBD. The microbial studies have elaborated the normal composition of the gut microbiome and its perturbations in the setting of IBD. This altered microbiome or "dysbiosis" is a key player in the protracted course of inflammation in IBD. Numerous genome-wide association studies have identified further genes involved in gastrointestinal innate immunity (including polymorphisms in genes involved in autophagy: ATG16L1 and IGRM), which have helped elucidate the relationship of the local innate immunity with the adjacent luminal bacteria. These developments have also spurred the search for specific pathogens which may have a role in the metamorphosis of the gut microbiome from a symbiotic entity to a putative pathogenic one. Here we review advances in our understanding of microbial involvement in IBD pathogenesis over the past 10 years and offer insight into how this will shape our therapeutic management of the disease in the coming years.
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“In addition, alteration of the intestinal microbiota has been demonstrated to be a key player in the protracted course of inflammation in inflammatory bowel diseases (IBD) [22].”
From Intestinal Microbiota Is Influenced by Gender and Body Mass Index (2016) · cites this paper as [22]
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“A definitive change of the normal gut microbiota with a breakdown of host-microbial mutualism is probably the defining event in IBD development.59”
From The gut microbiota and host health: a new clinical frontier (2016) · cites this paper as [59]
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The gut microbiota and host health: a new clinical frontier
Marchesi, J. R., Adams, D. H., Fava, F., Hermes, G. D. A., Hirschfield, G. M., Hold, G., Quraishi, M. N., Kinross, J., Smidt, H., Tuohy, K. M., et al. (2016) · Gut · doi:10.1136/gutjnl-2015-309990 · Cited by 2,302
Self-citationTherapeutic Peptides: Current Applications and Future Directions
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Metadata
- Authors
- Hold, G. L.
- Affiliations
- University of Aberdeen (GB)
- Corresponding author
- Hold, Georgina L
- ORCID
- Hold, Georgina L
- Venue
- World Journal of Gastroenterology
- Publisher
- Baishideng Publishing Group Inc.
- Published
- 2014
- Volume
- 20
- Issue
- 5
- Pages
- 1192
- ISSN
- 1007-9327 (ISSN-L)
- PMC
- PMC3921503
- OpenAlex
- W2115524426
- Cited by
- 365
- References
- 235
- Citations by year
- 2026: 12 · 2025: 26 · 2024: 27 · 2023: 25 · 2022: 24 · 2021: 40 · 2020: 27 · 2019: 41 · 2018: 36 · 2017: 31 · 2016: 31 · 2015: 34 · 2014: 11
- FWCI
- 3.36
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- cc-by-nc
- Locations
- World Journal of Gastroenterology (publishedVersion, cc-by-nc)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Health Sciences › Medicine › Gastroenterology › Inflammatory Bowel Disease
- Health Sciences › Medicine › Gastroenterology › Microscopic Colitis
- Keywords
- gut microbiota, inflammatory bowel disease, Crohn's disease, dysbiosis, NOD2, susceptibility genes, innate immunity, autophagy, ATG16L1, pathogen identification
- MeSH terms
- Animals, Bacteria, Colitis, Ulcerative, Crohn Disease, Humans, Immunity, Innate, Intestines, Phenotype, Risk Factors, Immunity, Mucosal, Genetic Predisposition to Disease, Polymorphism, Single Nucleotide, Microbiota, Dysbiosis
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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