The association between corneal immune cell dynamics and comfort in silicone hydrogel contact lens wearers.

Abstract

Purpose: To study the association between corneal immune cell dynamics and contact lens (CL) comfort, as well as tear film inflammatory mediators in established CL wearers.

Methods: A prospective, cross-sectional study including existing CL wearers was conducted. Symptoms were assessed with a comfort visual analog scale (VAS) and the Contact Lens Dry Eye Questionnaire-8. In-vivo corneal confocal microscopy was used to track immune cell dynamics over 3 timepoints at 5-minute intervals. Trajectory speed was calculated as the total length travelled by cells divided by time; displacement speed as the straight-line distance between the start and end positions of a cell divided by time; and persistence ratio as the ratio of displacement speed and trajectory speed. Measurements were performed for 1-3 cells per participant, and the minimum, maximum, and average values were analyzed. Tear film samples were collected to assess matrix metalloproteinase (MMP)-9, tissue inhibitor of metalloproteinase (TIMP)-1, and the MMP-9/TIMP-1 ratio. Correlations between immune cell dynamics, symptoms, and tear inflammatory mediators, were analyzed.

Results: Nineteen CL wearers (4 men and 15 women) aged 30 ± 5 years were included. Participants wore silicone hydrogel CLs for 8-10 h before clinical assessment. There was a significant association between comfort VAS and the maximum (rho = 0.533; p = 0.019) and average (rho = 0.506; p = 0.027) values of immune cell displacement speed. The concentration of MMP-9 was associated with the minimum value of trajectory speed (rho = 0.621; p = 0.031). Finally, the MMP-9/TIMP-1 ratio was associated with the maximum value of trajectory speed (rho = -0.717; p = 0.030), and the maximum (rho = -0.720; p = 0.008) and average (rho = -0.678; p = 0.015) values of displacement speed.

Conclusion: Corneal immune cell dynamics is related to sensations of discomfort in silicone hydrogel CL wearers, with cell speed possibly being regulated by inflammatory mediators assessed from the tear film. These observations may aid in understanding the mechanisms underlying the discomfort response.