Abstract
Purpose :
Cytomegalovirus (CMV) associated anterior segment infection is a new disease entity in immunocompetent patients. One of important clinical presentation is elevation of intraocular pressure (IOP), though the mechanism remains unclear. This study aimed to investigate the possible pathogenesis of IOP elevation in cytomegalovirus infection using in vivo models.
Methods :
Primary infection model of CMV trabeculiitis was established by intracameral injection of rat CMV on sex-week-old male Sprague Dawley rats. The intraocular pressure was recorded using TonoLab after infection. The aqueous humor and drainage lymph nodes were collected and analyzed using flow cytometry since at post-infection day 1, day 2, day 6, and day 14. Analysis of cytokine and chemokine from aqueous humor was measured by Milliplex. The histopathology of angle section was processed and immunostaining with immediate early CMV antigen.
Results :
A significant IOP elevation for 2 weeks was found in CMV-infected eyes, comparing to MOCK eyes. The amount of elevation was correlated to virus titer. At day 1 and day 2, CMV infection significantly increased expression of MCP-1 and IL-1β. The innate response with NK cells, CD11bc cells was evidenced by flow cytometry. MCP-1 receptor antagonist significantly decreased IOP elevation. At day 6, The T cell response with CD4 T cells, CD8 T cells, NKT cells took place. CMV infection significantly increased expression of IL-6, TGF-β1, and TGF-β2. Prominent cell infiltration and meshwork destruction could be observed in CMV-infected eyes. At day 14, cell response decreased along with decrement of IOP.
Conclusions :
In acute stage, CMV triggers cytokines to recruit inflammatory cells and causes IOP elevation in trabeculiitis. Permenant destruction of trabecular meshwork and reduction of extracellular matrix turnover by TGF-β may explain the poor IOP control in chronic cases.
This is a 2020 ARVO Annual Meeting abstract.