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Updated: Feb 1, 2026

A Mouse Model for Pathogen-induced Chronic Inflammation at Local and Systemic Sites
Published on: August 8, 2014
VIP modulates the ALX/FPR2 receptor axis toward inflammation resolution in a mouse model of bacterial keratitis
Thomas W Carion1, David Kracht1, Eliisa Strand1
1Department of Ophthalmology, Visual & Anatomical Sciences, Wayne State University School of Medicine, Detroit, MI 48201, United States.
Abstract:
Vasoactive intestinal peptide (VIP) has been shown to regulate corneal inflammation. Formyl peptide receptor 2 (FPR2) is a transmembrane protein belonging to the GPCR family. Ligands include pro-resolving lipids, lipoxin A4 (LXA4) and resolvin D1 (RvD1). The current study focuses on the effect of VIP regarding the FPR2 receptor axis in improving disease outcome in a mouse model of bacterial keratitis. Infection was induced in C57BL/6 (B6) mice using P. aeruginosa (PA) ATCC 19660. Mice received topical treatment (VIP or PBS) 3× daily after infection. Mean clinical scores, bacterial plate counts, Griess and myeloperoxidase (MPO) assays indicate that topical VIP effectively abrogates the disease response. Findings also reveal that VIP influences FPR2 pathway activation independent of archetypal VIP receptors. Exploring the immunoresolving role of FPR2, its ligand RvD1 and related enzymes (5-LOX, 12/15-LOX), our results suggest a mechanism by which VIP treatment influences the disease response in bacterial keratitis, which could offer a therapeutic point of intervention for enhancing this pro-resolving circuit.
Insights
Vasoactive intestinal peptide (VIP) treatment effectively reduces bacterial keratitis severity in mice. This peptide influences the formyl peptide receptor 2 (FPR2) pathway, offering a potential therapeutic strategy for eye infections.
Area of Science:
- Ophthalmology
- Immunology
- Pharmacology
Background:
- Corneal inflammation is a significant cause of vision impairment.
- Vasoactive intestinal peptide (VIP) is known to modulate inflammatory processes.
- Formyl peptide receptor 2 (FPR2) is implicated in inflammation resolution.
Purpose of the Study:
- To investigate the therapeutic potential of VIP in bacterial keratitis.
- To elucidate the role of the VIP-FPR2 axis in disease outcome.
- To explore VIP's mechanism of action in resolving inflammation.
Main Methods:
- Bacterial keratitis was induced in C57BL/6 mice using Pseudomonas aeruginosa.
- Mice received topical VIP or PBS treatment post-infection.
- Clinical scores, bacterial load, and inflammatory markers (Griess, MPO) were assessed.
Main Results:
- Topical VIP treatment significantly reduced clinical scores and bacterial counts.
- VIP treatment effectively abrogated the inflammatory disease response.
- VIP's effects on FPR2 pathway activation were observed independently of canonical VIP receptors.
Conclusions:
- VIP demonstrates therapeutic efficacy in a mouse model of bacterial keratitis.
- VIP influences the FPR2 pathway, suggesting a novel immunoresolving mechanism.
- Targeting the VIP-FPR2 axis presents a potential therapeutic intervention for bacterial keratitis.
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