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Tohru Sakimoto, Satoshi Sugaya, Takako Ohnishi, Akiko Ishimori, Mitsuru Sawa; Anti-inflammatory Effect of IL-6 Receptor Blockade on Experimental Corneal Alkali Burn. Invest. Ophthalmol. Vis. Sci. 2012;53(14):4206.
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We investigated the effect of IL-6R blockade on the corneal inflammation due to alkali burn.
Corneal alkali burn was made from a filter paper dipped in 1 N NaOH solution using BALB/c mice. Ten eyes of 10 mice were treated by topical instillation of anti-IL-6R antibody solution (MR16-1, 2 µg/µL) from day 5 to day 28 after wounding. (MR16-1 group) The control group (12 eyes of 12 mice, PBS group) underwent topical 0.01M PBS (pH 7.4) solution. The photographs of the cornea were taken on day 28 and the areas of corneal neovascularization (vascularized area/total corneal area) were quantified. The mice were euthanatized on day 28 and the expression of phosphorylated signal transducer and activator of transcription 3 (STAT3), Gr-1 (neutrophil marker), and F4/80 (macrophage marker) in the cornea was evaluated by immunohistochemistry. The cells with positive staining in the corneal stroma were counted.
On day 28 after the alkali burn treatment, vascularized area was significantly reduced in MR16-1 group (MR16-1 group; 50.3±8.2 %, PBS group; 79.8±14.6 %,)(P<0.05). The number of positive-cells in corneal stroma for phosphorylated STAT3 (PBS group; 32.9±8.3 cells/field, MR16-1 group; 17.0±3.1 cells/field)(P<0.01), Gr-1 (PBS group; 44.8±11.1 cells/field, MR16-1 group; 13.3±4.5 cells/field)(P<0.01), and F4/80 (PBS group; 68.5±15.7 cells/field, MR16-1 group; 40.0±5.4 cells/field)(P<0.05) were significantly fewer in MR16-1 group than those in PBS group on day 28.
In the corneal alkali burn, the corneal neovascularization, infiltration of neutrophils and macrophages and the positive-cells for phospholylated STAT3, an inflammatory signal-transducing protein located downstream of IL-6 signaling, were inhibited by topical instillation of MR16-1. These results indicate the blockade of IL-6R contributes to suppress corneal inflammatory response.
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