May 2003
Volume 44, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2003
Analysis of Cauterization-induced Corneal Inflammation in CCR2KO Mice
Author Affiliations & Notes
  • T. Oshima
    Ophthalmology, Kyushu Univ Sch of Med, Fukuoka, Japan
  • K. Sonoda
    Ophthalmology, Kyushu Univ Sch of Med, Fukuoka, Japan
  • C. Tsutsumi
    Ophthalmology, Kyushu Univ Sch of Med, Fukuoka, Japan
  • H. Qiao
    Ophthalmology, Kyushu Univ Sch of Med, Fukuoka, Japan
  • T. Ishibashi
    Ophthalmology, Kyushu Univ Sch of Med, Fukuoka, Japan
  • Footnotes
    Commercial Relationships  T. Oshima, None; K. Sonoda, None; C. Tsutsumi, None; H. Qiao, None; T. Ishibashi, None.
Investigative Ophthalmology & Visual Science May 2003, Vol.44, 1390. doi:
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    • Get Citation

      T. Oshima, K. Sonoda, C. Tsutsumi, H. Qiao, T. Ishibashi; Analysis of Cauterization-induced Corneal Inflammation in CCR2KO Mice . Invest. Ophthalmol. Vis. Sci. 2003;44(13):1390.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Abstract: : Purpose: C-C chemokine receptor (CCR) 2 induces monocyte chemotaction via interaction with it’s ligand such as Monocyte chemoattractant protein-1. CCR2 is well known to play an important role in monocyte and macrophage infiltration. The object of this study was to elucidate the role of CCR2 on corneal inflammation. Methods: We used a cauterization-induced corneal inflammation model. The corneas of CCR2 knockout (KO) mice and control mice were cauterized with silver nature (1 mm in diameter). Clinical signs such as corneal edema, opacity, and corneal neovascularization, which are major causes of visual disturbance, were examined 96 hours after cauterization. The corneal edema and opacity were clinically scored under a stereoscopic microscope. The corneal neovascularization was evaluated by the length of the blood vessels from the limbus and the sum of extension central angle of vasularized limbus. Furthermore, the phenotypes of the cornea-infiltrating cells were analyzed by flow cytometry. Results: In control mouse, flow cytometric analysis revealed that most of the infiltrating cells were neutrophils and macrophages. In contrast, the corneal infiltration of macrophages was impaired in CCR2KO mice. Instead of macrophages, prominent neutrophil infiltration was observed at cornea in CCR2KO mice. Both control and KO mice corneas showed same level of edema, neovasculization and opacity. Conclusions: The neutrophils compensate the macrophage function and induce same level of corneal inflammation in CCR2 KO mice.

Keywords: cornea: basic science • inflammation • cytokines/chemokines 
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