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Inhibition of Corneal Inflammation by the Resolvin E1
Ji-Eun Lee1, Yan Sun2, Per Gjorstrup3
1Department of Ophthalmology and Visual Sciences Case Western Reserve University, Cleveland, Ohio, United States.
Purpose:
To investigate the role of the lipid mediator, resolvin E1 (RvE1), in corneal inflammation.
Methods:
The effect of RvE1 on stimulated human corneal epithelial cells (HCECs) and neutrophils, and mouse macrophage was assessed. C57BL/6 mouse corneas were abraded and treated with RvE1 either before or after stimulation with lipopolysaccharide (LPS) and antibiotic-killed Pseudomonas aeruginosa and Staphylococcus aureus. The levels of CXC chemokines in the cornea were quantified, and the presence of neutrophils in corneal infiltrates was detected by immunohistochemistry and by in vivo confocal microscopy. The effect of RvE1 on apoptosis in the corneal epithelium was assessed using the TUNEL assay.
Results:
RvE1 significantly inhibited cytokine production in HCECs and neutrophils, and mouse macrophages and cornea. The development of corneal infiltrates, specifically neutrophils, in response to stimulation with LPS, P. aeruginosa, and S. aureus was also significantly reduced. There was no apoptotic effect of RvE1 on mouse corneal epithelial cells.
Conclusions:
RvE1 inhibits corneal inflammation induced by LPS, Gram negative (P. aeruginosa) and Gram positive (S. aureus) bacteria. These findings indicate that RvE1 as a potential anti-inflammatory therapy for patients with corneal inflammation and also, when given together with antibiotics, for bacterial keratitis.
Insights
Resolvin E1 (RvE1) reduces corneal inflammation by inhibiting cytokine production and neutrophil infiltration. This lipid mediator shows potential as an anti-inflammatory therapy for bacterial keratitis.
Area of Science:
- Ophthalmology
- Immunology
- Pharmacology
Background:
- Corneal inflammation is a significant cause of vision impairment.
- Lipid mediators play crucial roles in regulating inflammatory responses.
- Resolvin E1 (RvE1) is an endogenous lipid mediator with known anti-inflammatory properties.
Purpose of the Study:
- To investigate the therapeutic potential of RvE1 in corneal inflammation.
- To determine RvE1's effect on key inflammatory mediators and cellular responses in the cornea.
Main Methods:
- Assessed RvE1's impact on human corneal epithelial cells (HCECs), neutrophils, and mouse macrophages.
- Administered RvE1 to mouse corneas stimulated with lipopolysaccharide (LPS) and bacteria (P. aeruginosa, S. aureus).
- Quantified chemokine levels, neutrophil infiltration (immunohistochemistry, in vivo confocal microscopy), and apoptosis (TUNEL assay).
Main Results:
- RvE1 significantly inhibited cytokine production in HCECs, neutrophils, macrophages, and corneal tissue.
- RvE1 markedly reduced neutrophil infiltration in response to LPS and bacterial challenge.
- No apoptotic effects of RvE1 were observed in mouse corneal epithelial cells.
Conclusions:
- RvE1 effectively suppresses corneal inflammation induced by LPS and Gram-positive/negative bacteria.
- RvE1 demonstrates promise as an anti-inflammatory therapeutic for corneal conditions.
- RvE1 may be beneficial in combination with antibiotics for treating bacterial keratitis.
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