Intestinal barrier dysfunction in inflammatory bowel diseases
Open accessAbstract
The etiology of human inflammatory bowel diseases (IBDs) is believed to involve inappropriate host responses to the complex commensal microbial flora in the gut, although an altered commensal flora is not completely excluded. A multifunctional cellular and secreted barrier separates the microbial flora from host tissues. Altered function of this barrier remains a major largely unexplored pathway to IBD. Although there is evidence of barrier dysfunction in IBD, it remains unclear whether this is a primary contributor to disease or a consequence of mucosal inflammation. Recent evidence from animal models demonstrating that genetic defects restricted to the epithelium can initiate intestinal inflammation in the presence of normal underlying immunity has refocused attention on epithelial dysfunction in IBD. We review the components of the secreted and cellular barrier, their regulation, including interactions with underlying innate and adaptive immunity, evidence from animal models of the barrier's role in preventing intestinal inflammation, and evidence of barrier dysfunction in both Crohn's disease and ulcerative colitis.
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Excessive fragmentation and vascularization are characteristic dysfunction of ER and Golgi networks and observed in intestinal mucosa of ulcerative colitis patients.
“Notably, the excessive fragmentation and vascularization are the characteristic dysfunction of the ER and the Golgi networks and observed in the intestinal mucosa of UC patients [202].”
From Insights of Endocytosis Signaling in Health and Disease (2023) · cites this paper as [202]
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- Authors
- McGuckin, M. A., Eri, R., Simms, L. A., Florin, T. H. J., & Radford-Smith, G.
- Affiliations
- Mater Health Services (AU)
- QIMR Berghofer Medical Research Institute (AU)
- Venue
- Inflammatory Bowel Diseases
- Publisher
- Oxford University Press (OUP)
- Published
- 2009-01
- Volume
- 15
- Issue
- 1
- Pages
- 100-113
- ISSN
- 1078-0998 (ISSN-L)
- OpenAlex
- W2101203073
- Cited by
- 627
- References
- 6
- Citations by year
- 2026: 22 · 2025: 36 · 2024: 25 · 2023: 52 · 2022: 40 · 2021: 35 · 2020: 41 · 2019: 32 · 2018: 38 · 2017: 35 · 2016: 36 · 2015: 37 · 2014: 38 · 2013: 28 · 2012: 50
- FWCI
- 2.62
- Type
- journal article
- Language
- en
- Open access
- green
- figshare.com
- Licence
- cc-by
- Locations
- Inflammatory Bowel Diseases (publishedVersion)
- PubMed (publishedVersion)
- eCite Digital Repository (University of Tasmania) (submittedVersion)
- Figshare (submittedVersion, cc-by)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Inflammatory Bowel Disease
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Health Sciences › Medicine › Gastroenterology › Gastrointestinal motility and disorders
- Keywords
- intestinal barrier dysfunction, Crohn's disease
- MeSH terms
- Animals, Humans, Intestinal Mucosa, Permeability, Inflammatory Bowel Diseases, Bacterial Translocation
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