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Updated: Aug 8, 2025

Chronic Salmonella Infection Induced Intestinal Fibrosis
Published on: September 22, 2019
hucMSC-Ex Alleviates IBD-Associated Intestinal Fibrosis by Inhibiting ERK Phosphorylation in Intestinal Fibroblasts
Yifei Wang1,2, Yaqin Zhang1,2, Bing Lu3
1Wujin Institute of Molecular Diagnostics and Precision Cancer Medicine of Jiangsu University, Jiangsu University, 213017 Changzhou, China.
Human umbilical cord mesenchymal stem cell-derived exosomes (hucMSC-Ex) alleviate intestinal fibrosis in IBD models. These exosomes inhibit fibroblast activity by reducing ERK phosphorylation, offering a potential new treatment for IBD-related fibrosis.
Area of Science:
- Gastroenterology
- Regenerative Medicine
- Cell Biology
Background:
- Intestinal fibrosis is a severe complication of inflammatory bowel disease (IBD), leading to fistula and stricture formation.
- Current treatments for IBD-related fibrosis are lacking.
- Mesenchymal stem cell-derived exosomes show promise in treating organ fibrosis.
Purpose of the Study:
- To investigate the therapeutic potential of human umbilical cord mesenchymal stem cell-derived exosomes (hucMSC-Ex) in IBD-related intestinal fibrosis.
- To elucidate the underlying mechanism of hucMSC-Ex in mitigating intestinal fibrosis.
Main Methods:
- Established a DSS-induced mouse model of IBD-related intestinal fibrosis.
- Utilized TGF-β-induced human intestinal fibroblasts (CCD-18Co) to assess hucMSC-Ex effects.
- Investigated the role of the extracellular-signal-regulated kinase (ERK) pathway and employed an ERK inhibitor.
Main Results:
- hucMSC-Ex treatment reduced intestinal wall thickness and fibrosis markers in the mouse model.
- hucMSC-Ex inhibited TGF-β-induced proliferation, migration, and activation of human intestinal fibroblasts.
- ERK phosphorylation was identified as a key mediator, with its inhibition decreasing fibrosis indicators (α-SMA, fibronectin, collagen I).
Conclusions:
- hucMSC-Ex effectively alleviates DSS-induced IBD-related intestinal fibrosis.
- The mechanism involves inhibiting profibrotic molecules and fibroblast activity via decreased ERK phosphorylation.
- hucMSC-Ex presents a novel therapeutic strategy for IBD-associated intestinal fibrosis.
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