Abstract
Purpose :
To develop a desiccating stress-induced dry eye disease model using nonhuman primates (NHP).
Methods :
Four to 5-year-old Rhesus macaque monkeys were housed in a controlled-environment room where relative humidity (RH), temperature (T) and airflow (AF) are regulated (RH = 6.4% ± 1.4%, T = 22.5°C - 25.3°C, AF = 12 L/min). Monkeys were placed in the controlled-environment room for 21 to 36 days to induce dry eye disease (DED). Post 21 days of DED induction, corneas were topically treated with 1 % Pred Forte or normal saline (placebo) thrice daily for 14 days. Corneal fluorescein staining (CFS), tear film break-up time (TFBUT), and proinflammatory cytokines in tears were measured to assess DED severity.
Results :
A significant increase in corneal fluorescein staining (9.7 ± 1.8, P < 0.001) and proinflammatory cytokines levels (IL-17, P < 0.01; IL-2, P < 0.05) were observed on day 21 of controlled-environment room exposure. Moreover, TFBUT significantly decreased following DED induction (7.3 ± 2.4 vs. 4.4 ± 0.8, P < 0.001). Corticosteroid treatment significantly reduced CFS scoring (6.0 ± 1.2 vs. 9.3 ± 1.8, P < 0.001), restored TFBUT (6.1 ± 2.0 vs. 3.9 ± 0.6, P = 0.001), and prevented upregulation of tear proinflammatory cytokines, compared to the placebo treatment.
Conclusions :
Desiccating stress induces dry eye disease in nonhuman primates, closely resembling the clinical symptoms and treatment response observed in human DED patients.
This abstract was presented at the 2022 ARVO Annual Meeting, held in Denver, CO, May 1-4, 2022, and virtually.