Abstract
Abstract: :
Purpose: The inflammatory response is thought to play a role in the laser–induced model of choroidal neovascularization (CNV). We examined the role of anti–inflammatory cytokine IL–10 in this model. Methods: Rupture of Bruch’s membrane with krypton red laser was used to initiate CNV in C57Bl/6 mice and age–matched IL–10–/– mice. Four burns were placed around the optic nerve (50 microns, 0.05 seconds, 280 mW). One week after laser, the mice were perfused with FITC–labeled dextran, and choroidal flat mounts were prepared for analysis of CNV using confocal microscopy. Bone marrow chimeras were generated to determine if relevant IL–10 was produced by hematopoietic or non–hematopoietic cells. Results: IL–10 KO mice have a 50–60% reduction in the incidence and volume of CNV compared to wild type mice. CNV in IL–10–/– mice with wild type hematopoietic cells resembled wild type, while CNV in wild type mice with IL–10–/– hematopoietic cells resembled IL–10–/– mice. Conclusions: Loss of the anti–inflammatory cytokine IL–10 from hematopoietic cells did not lead to increased CNV but resulted in a significant reduction in neovascularization. This suggests that IL–10 may play a positive role in CNV and/or that the role of the inflammatory response in laser induced CNV is much more complex than currently believed.
Keywords: choroid: neovascularization • age–related macular degeneration • inflammation