ArticlePloS one2015
The intestinal barrier in irritable bowel syndrome: subtype-specific effects of the systemic compartment in an in vitro model.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 21 citations in OpenAlex.
- Reframing precision nutrition in irritable bowel syndrome: a mechanism-informed conceptual framework for responder prediction and clinical translation.Frontiers in immunology · 2026Review
- Gut microbial dysbiosis associated to diarrheic irritable bowel syndrome can be efficiently simulated in the Mucosal ARtificial COLon (M-ARCOL).Bioengineered · 2025Article
- Electroacupuncture restores intestinal mucosal barrier in IBS-D rats by modulating mast cell-derived exosomal MiR-149-5p.Frontiers in immunology · 2025Article
- Fecal luminal factors from patients with irritable bowel syndrome induce distinct gene expression of colonoids.Neurogastroenterology and motility · 2022Article
- High FODMAP diet causes barrier loss via lipopolysaccharide-mediated mast cell activation.JCI insight · 2021Article
- Cx43 and the Actin Cytoskeleton: Novel Roles and Implications for Cell-Cell Junction-Based Barrier Function Regulation.Biomolecules · 2020Review
- Presentation and Characteristics of Abdominal Pain Vary by Irritable Bowel Syndrome Subtype: Results of a Nationwide Population-Based Study.The American journal of gastroenterology · 2020Article
- Increasing Evidence That Irritable Bowel Syndrome and Functional Gastrointestinal Disorders Have a Microbial Pathogenesis.Frontiers in cellular and infection microbiology · 2020Review
- The Microbiome and Irritable Bowel Syndrome - A Review on the Pathophysiology, Current Research and Future Therapy.Frontiers in microbiology · 2019Review
- Activation of Eosinophils and Mast Cells in Functional Dyspepsia: an Ultrastructural Evaluation.Scientific reports · 2018Article
- Decreased TESK1-mediated cofilin 1 phosphorylation in the jejunum of IBS-D patients may explain increased female predisposition to epithelial dysfunction.Scientific reports · 2018Article
- FODMAP diet modulates visceral nociception by lipopolysaccharide-mediated intestinal inflammation and barrier dysfunction.The Journal of clinical investigation · 2018Article
- Article
- A Novel, Nonpeptidic, Orally Active Bivalent Inhibitor of Human β-Tryptase.Pharmacology · 2018Article
- Alpha-ketoglutarate suppresses the NF-κB-mediated inflammatory pathway and enhances the PXR-regulated detoxification pathway.Oncotarget · 2017Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIrritable bowel syndrome (IBS) is a disorder with multifactorial pathophysiology. Intestinal barrier may be altered, especially in diarrhea-predominant IBS (IBS-D). Several mediators may contribute to increased intestinal permeability in IBS.
aimWe aimed to assess effects of tryptase and LPS on in vitro permeability using a 3-dimensional cell model after basolateral cell exposure. Furthermore, we assessed the extent to which these mediators in IBS plasma play a role in intestinal barrier function. MATERIALS AND
methodsCaco-2 cells were grown in extracellular matrix to develop into polarized spheroids and were exposed to tryptase (10 - 50 mU), LPS (1 - 50 ng/mL) and two-fold diluted plasma samples of 7 patients with IBS-D, 7 with constipation-predominant IBS (IBS-C) and 7 healthy controls (HC). Barrier function was assessed by the flux of FITC-dextran (FD4) using live cell imaging. Furthermore, plasma tryptase and LPS were determined.
resultsTryptase (20 and 50 mU) and LPS (6.25 - 50 ng/mL) significantly increased Caco-2 permeability versus control (all P< 0.05). Plasma of IBS-D only showed significantly elevated median tryptase concentrations (7.1 [3.9 - 11.0] vs. 4.2 [2.2 - 7.0] vs. 4.2 [2.5 - 5.9] μg/mL; P<0.05) and LPS concentrations (3.65 [3.00 - 6.10] vs. 3.10 [2.60-3.80] vs. 2.65 [2.40 - 3.40] EU/ml; P< 0.05) vs. IBS-C and HC. Also, plasma of IBS-D increased Caco-2 permeability versus HC (0.14450 ± 0.00472 vs. 0.00021 ± 0.00003; P < 0.001), which was attenuated by selective inhibition of tryptase and LPS (P< 0.05).
conclusionBasolateral exposure of spheroids to plasma of IBS-D patients resulted in a significantly increased FD4 permeation, which was partially abolished by selective inhibition of tryptase and LPS. These findings point to a role of systemic tryptase and LPS in the epithelial barrier alterations observed in patients with IBS-D.
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