T Suzuki1, Y Sano, S Kinoshita. 1. Department of Ophthalmology, Kyoto Prefectural University of Medicine, Japan. tsuzuki@ophth.kpu-m.ac.jp
Abstract
PURPOSE: To examine the effects of 1alpha,25-dihydroxyvitamin D3 (1alpha,25[OH]2D3), a hormone that has immunosuppressive properties, on Langerhans cell (LC) migration and corneal neovascularization in mouse corneas. METHODS: Two 10-0 nylon interrupted sutures were placed in the center of 50 BALB/c mouse corneas to induce LC migration and corneal neovascularization. The mice were then randomly assigned to one of five groups. Three groups (n = 11, n = 11, n = 6) received topical 1alpha,25(OH)2D3 (at concentrations of 10(-7) M, 10(-)8 M, 10(-9) M), one group (n = 11) received vehicle only, and one group (n = 11) received no eye drops. Instillation (three times a day) began on the first day after suturing. Corneal neovascularization was assessed by slit lamp microscopy and scored according to the length of newly formed corneal vessels. Fourteen days after suturing, the number of LCs that had migrated into the central corneal epithelium was counted by an immunofluorescence assay using an anti-Ia antibody. RESULTS: The number of LCs in the central cornea was 21.9 +/- 2.8 cells/mm2 in the nontreated group and 17.8 +/- 3.9 cells/mm2 in the vehicle-only group. Significantly fewer LCs were detected in all groups that had received 1alpha,25(OH)2D3 compared with the vehicle only and nontreated groups (10(-7) M: 7.4 +/- 1.2 cells/mm2, 10(-8) M: 7.2 +/- 2.0 cells/mm2, 10(-9) M: 6.2 +/- 0.7 cells/mm2). Moderate inhibition of corneal vascularization was observed in the 10(-7) M 1alpha,25(OH)2D3 group, but not the other groups. CONCLUSIONS: Topical administration of 1alpha,25(OH)2D3 can be effective in suppressing ocular surface inflammation by inhibiting LC migration into mouse corneas.
PURPOSE: To examine the effects of 1alpha,25-dihydroxyvitamin D3 (1alpha,25[OH]2D3), a hormone that has immunosuppressive properties, on Langerhans cell (LC) migration and corneal neovascularization in mouse corneas. METHODS: Two 10-0 nylon interrupted sutures were placed in the center of 50 BALB/c mouse corneas to induce LC migration and corneal neovascularization. The mice were then randomly assigned to one of five groups. Three groups (n = 11, n = 11, n = 6) received topical 1alpha,25(OH)2D3 (at concentrations of 10(-7) M, 10(-)8 M, 10(-9) M), one group (n = 11) received vehicle only, and one group (n = 11) received no eye drops. Instillation (three times a day) began on the first day after suturing. Corneal neovascularization was assessed by slit lamp microscopy and scored according to the length of newly formed corneal vessels. Fourteen days after suturing, the number of LCs that had migrated into the central corneal epithelium was counted by an immunofluorescence assay using an anti-Ia antibody. RESULTS: The number of LCs in the central cornea was 21.9 +/- 2.8 cells/mm2 in the nontreated group and 17.8 +/- 3.9 cells/mm2 in the vehicle-only group. Significantly fewer LCs were detected in all groups that had received 1alpha,25(OH)2D3 compared with the vehicle only and nontreated groups (10(-7) M: 7.4 +/- 1.2 cells/mm2, 10(-8) M: 7.2 +/- 2.0 cells/mm2, 10(-9) M: 6.2 +/- 0.7 cells/mm2). Moderate inhibition of corneal vascularization was observed in the 10(-7) M 1alpha,25(OH)2D3 group, but not the other groups. CONCLUSIONS: Topical administration of 1alpha,25(OH)2D3 can be effective in suppressing ocular surface inflammation by inhibiting LC migration into mouse corneas.