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T. Oshima, K.–H. Sonoda, C. Tsutsumi–Miyahara, T. Hisatomi, S. Hamano, B.J. Rollins, T. Ishibashi; Analysis of Cauterization–Induced Corneal Inflammation in MCP–1 Knockout Mice . Invest. Ophthalmol. Vis. Sci. 2005;46(13):2647.
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Purpose: Monocyte chemotactic protein (MCP)–1 induces monocyte/macrophage migration to the inflammatory lesions via interaction with it’s receptor C–C chemokine receptor (CCR)2 . Several reports have demonstrated the role of macrophages in corneal inflammation. The object of this study was to elucidate the role of MCP–1 on corneal inflammation. Methods: We used a cauterization–induced corneal inflammation model. The corneas of MCP–1 knockout (KO) mice and control mice were cauterized with silver nature (1 mm in diameter). Clinical signs such as corneal edema and opacity were examined 96 hours after cauterization. Furthermore, the phenotypes of the cornea–infiltrating cells were analyzed by flow cytometry. We also examined the corneal inflammation in neutrophil–depleted mice. Results: In control mice, flow cytometric analysis revealed that most of the infiltrating cells were neutrophils and macrophages. The corneal infiltration of macrophages was impaired in MCP–1KO mice. Prominent neutrophil–infiltration was observed at cornea in MCP–1KO mice. Both control and KO mice corneas showed equivalent level of edema and opacity. In contrast, the depletion of neutrophils leads to significantly less edema and opacity. Conclusions: The neutrophils compensate the macrophage function and induce same level of corneal inflammation in MCP–1 KO mice.
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