coculture with intraocular lens materialactivated macrophages induces an inflammatory phenotype in lens epithelial cells cataracts are the leading cause of blindness worldwide requiring surgical implantation of an intraocular lens despite evidence of leukocyte ingress into the postoperative lens few studies have investigated the leukocyte response to intraocular lens materials a novel coculture model was developed to examine macrophage activation by hydrophilic acrylic poly2hydroxyethyl methacrylate and hydrophobic acrylic polymethylmethacrylate commercial intraocular lens the human monocytic cell line thp1 was differentiated into macrophages and cocultured with human lens epithelial cell line hleb3 with or without an intraocular lens for one two four or six days using flow cytometry and confocal microscopy expression of the macrophage activation marker cd54 intercellular adhesion molecule1 and production of reactive oxygen species via the fluorogenic probe 27dichlorodihydrofluorescein diacetate were examined in macrophages smooth muscle actin a transdifferentiation marker was characterized in lens epithelial cells the poly2hydroxyethyl methacrylate intraocular lens prevented adhesion but induced significant macrophage activation p003 versus control no intraocular lens while the polymethylmethacrylate intraocular lens enabled adhesion and multinucleated fusion but induced no significant activation coculture with either intraocular lens increased reactive oxygen species production in macrophages after one day p003 and increased expression of smooth muscle actin in hle b3 after six days although only poly2hydroxyethyl methacrylate induced a significant difference versus control p001 our results imply thatcontrary to prior uveal biocompatibility understandingmacrophage adherence is not necessary for a strong inflammatory response to an intraocular lens with hydrophilic surfaces inducing higher activation than hydrophobic surfaces these findings provide a new method of inquiry into uveal biocompatibility specifically through the quantification of cellsurface markers of leukocyte activation