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Targeting the Eph/Ephrin System as Anti-Inflammatory Strategy in IBD
Andrea Grandi1, Irene Zini1, Simone Palese1
1Food and Drug Department, University of Parma, Parma, Italy.
Frontiers in Pharmacology
|July 13, 2019
Summary
The EphB/ephrin-B system plays a role in gut inflammation. Blocking its forward signaling benefited TNBS colitis but not DSS colitis, suggesting a potential therapeutic target for inflammatory bowel diseases.
Area of Science:
- Molecular Biology
- Immunology
- Gastroenterology
Background:
- Erythropoietin-producing hepatocellular carcinoma type B (EphB) receptor tyrosine kinases and ephrin-B ligands are crucial for embryonic growth, cancer, immune responses, and intestinal integrity.
- These signaling pathways are implicated in the pathogenesis of inflammatory bowel diseases (IBDs).
- Understanding the EphB/ephrin-B system's role in intestinal inflammation is vital for developing new therapeutic strategies.
Purpose of the Study:
- To investigate the role of the EphB/ephrin-B system in intestinal inflammation.
- To assess the local and systemic effects of pharmacological manipulation of this system in mouse models of colitis.
- To evaluate the potential of EphB/ephrin-B blockade as a therapeutic target for IBDs.
Main Methods:
- Induced colitis in mice using 2,4,6-trinitrobenzenesulfonic acid (TNBS) and dextran sulphate sodium (DSS) models.
- Administered chimeric Fc-conjugated proteins (ephrin-B1-Fc, EphB1-Fc) to activate forward or reverse signaling, and EphB4 extracellular domain protein as an antagonist.
- Assessed inflammatory responses, splenic T lymphocyte subpopulations, and gene expression changes.
Main Results:
- Blockade of EphB/ephrin-B forward signaling was ineffective in DSS-induced colitis but showed beneficial effects in TNBS colitis.
- The blockade counteracted inflammatory responses and splenic T lymphocyte changes in TNBS colitis, independent of ephrin-B2 gene variant appearance.
- EphB4 administration promoted Tumor Necrosis Factor alpha (TNFα) release in vitro, suggesting complex immune modulation.
Conclusions:
- The EphB/ephrin-B system is a potential pharmacological target for intestinal inflammatory disorders.
- Therapeutic efficacy of EphB/ephrin-B blockade appears to involve immune response modulation.
- The mechanism of action is independent of changes in EphB4 and ephrin-B2 gene expression at the transcriptional and translational levels.
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