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Induction of Ocular Surface Inflammation and Collection of Involved Tissues
Published on: August 4, 2022
Interleukin-18 regulates pathological intraocular neovascularization
Hong Qiao1, Koh-Hei Sonoda, Yasuhiro Ikeda
1Ophthalmology, 3-1-1 Maidashi, Higashi-Ku, Fukuoka 812-8582, Japan.
Journal of Leukocyte Biology
|January 20, 2007
Summary
Interleukin-18 (IL-18) promotes the regression of abnormal retinal neovascularization (NV) in oxygen-induced retinopathy (OIR). This finding offers new therapeutic strategies for retinopathy in premature newborns.
Area of Science:
- Ophthalmology
- Immunology
- Developmental Biology
Background:
- The proinflammatory cytokine IL-18 is implicated in angiogenesis.
- Abnormal retinal neovascularization (NV) is a hallmark of retinopathy of prematurity.
- The specific role of IL-18 in retinal NV remains to be fully elucidated.
Purpose of the Study:
- To investigate the role of IL-18 in abnormal retinal neovascularization (NV) using an oxygen-induced retinopathy (OIR) mouse model.
- To determine whether IL-18 inhibits the development or promotes the regression of OIR.
Main Methods:
- Utilized a C57BL/6 mouse model of oxygen-induced retinopathy (OIR).
- Administered recombinant IL-18 and IL-18-binding protein during different phases of OIR.
- Quantified retinal neovascularization (NV) and IL-18 expression levels.
Main Results:
- IL-18 expression decreased during OIR development, coinciding with increased vascular endothelial growth factor (VEGF) and NV.
- IL-18 knockout mice exhibited more severe OIR that persisted longer.
- Administration of IL-18 during OIR development did not inhibit retinopathy, but neutralizing IL-18 during recovery prolonged OIR.
Conclusions:
- IL-18 negatively regulates retinal NV, primarily by promoting its regression rather than inhibiting its development.
- These findings suggest novel therapeutic approaches targeting IL-18 for treating human retinopathy of prematurity.
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