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Three-Dimensional Cell Culture Models to Investigate the Epithelial Barrier in Eosinophilic Esophagitis
Published on: May 10, 2024
CD98 positive eosinophils contribute to T helper 1 pattern inflammation
Fu-Min Xue1, Huan-Ping Zhang, Hui-Jie Hao
1Department of Gastroenterology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Plos One
|December 29, 2012
Summary
CD98(+) eosinophils (Eo) contribute to intestinal inflammation in inflammatory bowel disease (IBD). Flagellin (FGN) activates these cells via galectin 3, initiating inflammation and worsening colitis in mice.
Area of Science:
- Immunology
- Gastroenterology
- Cell Biology
Background:
- Inflammatory bowel disease (IBD) pathogenesis remains incompletely understood.
- Eosinophils (Eo) are key proinflammatory cells in chronic intestinal inflammation.
- CD98 is implicated in various inflammatory conditions.
Purpose of the Study:
- To investigate the role of CD98-expressing eosinophils (CD98(+) Eo) in initiating intestinal inflammation.
- To explore the involvement of flagellin (FGN) and galectin 3 in this process.
Main Methods:
- Immunohistochemistry on colon biopsies from 60 IBD patients.
- ELISA for serum flagellin (FGN) antibody and Eo-derived mediators.
- In vitro cell culture models to assess FGN's effect on Eo activation.
- In vivo mouse model to evaluate FGN's role in inducing colitis.
Main Results:
- CD98(+) Eo frequency was significantly higher in IBD colon mucosa compared to controls.
- FGN was detected in IBD colon biopsies and sera.
- FGN exposure increased galectin 3 expression in dendritic cells, activating CD98(+) Eo.
- Intrarectal FGN administration exacerbated colon inflammation in mice with eosinophilia.
Conclusions:
- The interaction between galectin 3 and CD98 activates eosinophils.
- This activation leads to the release of mediators that initiate intestinal inflammation.
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