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Endothelial barrier function and Na+/K(+)-ATPase pump density in herpetic stromal disease
W J O'Brien1, M L Palmer, J Guy
1Department of Ophthalmology, Medical College of Wisconsin, Milwaukee 53226, USA.
Investigative Ophthalmology & Visual Science
|January 1, 1996
Summary
Herpes simplex virus type 1 (HSV-1) infection reduces Na+/K+-ATPase pump density in the corneal endothelium, contributing to corneal edema. Barrier function remained intact during HSV-1-induced stromal disease.
Area of Science:
- Ophthalmology
- Virology
- Cell Biology
Background:
- Corneal edema is a key feature of herpes simplex virus type 1 (HSV-1) stromal disease.
- Corneal thickness relies on endothelial barrier function and Na+/K+-ATPase pumps regulating water movement.
Purpose of the Study:
- To investigate the roles of endothelial barrier function and Na+/K+-ATPase pump activity in HSV-1-induced corneal edema.
- To determine the contribution of these factors to the pathogenesis of edema.
Main Methods:
- Corneal edema and stromal disease were induced in rabbits via intrastromal HSV-1 injection.
- Endothelial barrier function and Na+/K+-ATPase pump sites were assessed at various time points post-infection.
Main Results:
- Endothelial permeability (Ktrans) remained unchanged during maximal corneal edema.
- A significant decrease in Na+/K+-ATPase pump density was observed during peak edema.
- Pump density normalized by 24 days post-infection, coinciding with edema resolution.
Conclusions:
- Corneal endothelial barrier function is not significantly altered in this HSV-1 stromal edema model.
- Reduced Na+/K+-ATPase pump density is a significant factor in the pathogenesis of HSV-1-induced corneal edema.
