ArticleScientific reports2015
Increased production of BDNF in colonic epithelial cells induced by fecal supernatants from diarrheic IBS patients.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 41 citations in OpenAlex.
- Somatization in patients with predominant diarrhoea irritable bowel syndrome: the role of the intestinal barrier function and integrity.BMC gastroenterology · 2021Trial
- Development of a novel humanized gut-brain axis model as a tool toward personalized nutrition.Communications biology · 2026Article
- Article
- 5-HTThe Journal of physiology · 2025Article
- Cytokines and Madness: A Unifying Hypothesis of Schizophrenia Involving Interleukin-22.International journal of molecular sciences · 2024Review
- Pomegranate Peel Extract Mitigates Diarrhea-Predominant Irritable Bowel Syndromes via MAPK and NF-κB Pathway Modulation in Rats.Nutrients · 2024Article
- Genetic Variations in TrkB.T1 Isoform and Their Association With Somatic and Psychological Symptoms in Individuals With IBS.The journal of pain · 2024Article
- Obligatory Activation of SRC and JNK by GDNF for Survival and Axonal Outgrowth of Postnatal Intestinal Neurons.Cellular and molecular neurobiology · 2022Article
- The Effect of Serine Protease Inhibitors on Visceral Pain in Different Rodent Models With an Intestinal Insult.Frontiers in pharmacology · 2022Article
- Local Colonic Administration of a Serine Protease Inhibitor Improves Post-Inflammatory Visceral Hypersensitivity in Rats.Pharmaceutics · 2021Article
- Electroacupuncture and Moxibustion Modulate the BDNF and TrkB Expression in the Colon and Dorsal Root Ganglia of IBS Rats with Visceral Hypersensitivity.Evidence-based complementary and alternative medicine : eCAM · 2021Article
- Blockade of BDNF signalling attenuates chronic visceral hypersensitivity in an IBS-like rat model.European journal of pain (London, England) · 2020Article
- Induction of brain-derived neurotrophic factor in enteric glial cells stimulated by interleukin-1β via a c-Jun N-terminal kinase pathway.Journal of clinical biochemistry and nutrition · 2020Article
- The Role of Brain-Derived Neurotrophic Factor in Irritable Bowel Syndrome.Frontiers in psychiatry · 2020Article
- Berberine prevents stress-induced gut inflammation and visceral hypersensitivity and reduces intestinal motility in rats.World journal of gastroenterology · 2019Article
- Protease Activated Receptor-2 Induces Immune Activation and Visceral Hypersensitivity in Post-infectious Irritable Bowel Syndrome Mice.Digestive diseases and sciences · 2019Article
- Diet Control More Intensively Disturbs Gut Microbiota Than Genetic Background in Wild Type and ob/ob Mice.Frontiers in microbiology · 2019Article
- Partners in Crime: NGF and BDNF in Visceral Dysfunction.Current neuropharmacology · 2019Review
- Neurotrophic factors in enteric physiology and pathophysiology.Neurogastroenterology and motility · 2018Review
- Newly developed serine protease inhibitors decrease visceral hypersensitivity in a post-inflammatory rat model for irritable bowel syndrome.British journal of pharmacology · 2018Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Colonic brain-derived neurotrophic factor (BDNF) plays an essential role in pathogenesis of abdominal pain in diarrhea-predominant irritable bowel syndrome (IBS-D), but regulation on its expression remains unclear. We investigated the role of fecal supernatants (FSN) from IBS-D patients on regulating BDNF expression in colonic epithelial cells of human and mice. Using human Caco-2 cells, we found that IBS-D FSN significantly increased BDNF mRNA and protein levels compared to control FSN, which were remarkably suppressed by the serine protease inhibitor. To further explore the potential mechanisms, we investigated the impact of protease-activated receptor-2 (PAR-2) on BDNF expression. We found a significant increase in PAR-2 expression in Caco-2 after IBS-D FSN stimulation. Knockdown of PAR-2 significantly inhibited IBS-D FSN-induced upregulation of BDNF. Moreover, we found that phosphorylation of p38 MAPK, not NF-κB p65, contributed to PAR-2-mediated BDNF overexpression. To confirm these results, we intracolonically infused IBS-D or control FSN in mice and found that IBS-D FSN significantly elevated colonic BDNF and visceral hypersensitivity in mice, which were both suppressed by the inhibitor of serine protease or antagonist of PAR-2. Together, our data indicate that activation of PAR-2 signaling by IBS-D FSN promotes expression of colonic BDNF, thereby contributing to IBS-like visceral hypersensitivity.
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