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Published on: July 10, 2018
Analysis of corneal inflammation induced by cauterisation in CCR2 and MCP-1 knockout mice
T Oshima1, K-H Sonoda, C Tsutsumi-Miyahara
1Department of Ophthalmology, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-Ku, Fukuoka, Japan.
Aim:
To elucidate the role of CCR2/MCP-1 in corneal inflammation.
Methods:
A cauterisation induced corneal inflammation model was used. The corneas were cauterised with silver nitrate in CCR2 knockout (KO) mice, MCP-1 KO mice, and control mice. Clinical signs such as corneal oedema and opacity were examined 96 hours after cauterisation and the phenotypes of the cells infiltrating the cornea were analysed by flow cytometry. Corneal inflammation in neutrophil depleted mice was also analysed.
Results:
After cauterisation both CCR2 KO and MCP-1 KO mice showed the same levels of corneal oedema and opacity as control mice. Flow cytometry revealed that in control mice most of the infiltrating cells were neutrophils and macrophages, whereas in both CCR2 KO mice and MCP-1 KO mice, the number of macrophages infiltrating the cornea were markedly reduced. However, prominent infiltrates of neutrophils were still observed in the cornea in CCR2 KO mice and MCP-1 KO mice. The depletion of neutrophils significantly reduced the oedema and opacity induced in the cornea by cauterisation.
Conclusion:
The CCR2 and MCP-1 molecules are not essential for cauterisation induced corneal inflammation. Neutrophils, rather than migrated macrophages, are the final effector cells involved in inducing inflammation in this model.
Insights
Chemokine (C-C motif) receptor 2 (CCR2) and its ligand, monocyte chemoattractant protein-1 (MCP-1), do not drive cauterization-induced corneal inflammation. Neutrophils, not macrophages, are key effector cells in this inflammatory model.
Area of Science:
- Ophthalmology
- Immunology
- Inflammation Research
Background:
- Corneal inflammation is a significant cause of vision impairment.
- The roles of chemokine (C-C motif) receptor 2 (CCR2) and its ligand, monocyte chemoattractant protein-1 (MCP-1), in ocular inflammation are not fully understood.
Purpose of the Study:
- To investigate the specific involvement of the CCR2/MCP-1 axis in a mouse model of cauterization-induced corneal inflammation.
Main Methods:
- A corneal cauterization model was established in wild-type, CCR2 knockout (KO), and MCP-1 KO mice.
- Clinical signs of inflammation (edema, opacity) were assessed 96 hours post-injury.
- Infiltrating immune cell populations were analyzed via flow cytometry.
- The impact of neutrophil depletion on corneal inflammation was evaluated.
Main Results:
- CCR2 KO and MCP-1 KO mice exhibited similar levels of corneal edema and opacity compared to controls.
- Macrophage infiltration was significantly reduced in CCR2 KO and MCP-1 KO mice.
- Neutrophil infiltration remained prominent in KO mice, and neutrophil depletion markedly reduced corneal edema and opacity.
Conclusions:
- The CCR2/MCP-1 pathway is not essential for the development of cauterization-induced corneal inflammation.
- Neutrophils, rather than recruited macrophages, are the primary effector cells driving inflammation in this model.
