Principal Investigator
Assistant Professor of Ophthalmology and Immunology
University of Pittsburgh School of Medicine
Publications
Contact Information
UPMC Vision Institute
UPMC Mercy Pavilion
1622 Locust Street
Pittsburgh, PA 15219
anthony.stleger@pitt.edu
Lab Personnel
Hongmin Yu, PhD, Research Assistant Professor
Alysha Slater, MS, Lab Manager
Jackie Shane, PhD, Postdoctoral Associate
Masaaki Yoshida, MD, Postdoctoral Associate
Julia Bierker, Technician
Ellen Fleming, Graduate Student
Research Focus
We have pioneered research in a historically understudied area of ophthalmology, the ocular microbiome and its effect(s) on ocular disease. Normally a highly contentious topic in ophthalmology, the ocular microbiome does indeed tune local immunity to prevent fungal and bacterial infection. Now, the St. Leger lab aims to extend those findings to explore how ocular resident bacteria may modulate immunity against viral infections like herpes simplex virus type 1 (HSV-1), which have the potential to cause blindness. To this end, the laboratory uses Corynebacterium masitidis as a candidate colonizer to explore how ocular immunity is developed and maintained. Further, the lab has a keen interest in understanding mechanisms controlling gd T cells, which are critical for the protection of the ocular surface from disease.
Future goals include the development of novel probiotic-like therapies for the treatment of diseases at the ocular surface. In addition, we are interested in how the local microbiome may affect intraocular diseases like glaucoma or age-related macular degeneration where the microbiome has been implicated but not proven for the development and progression of disease.
A separate arm of research in the laboratory focuses on investigating how corneal nerves affect the development of ocular disease. In healthy individuals, the cornea, which is the most densely innervated tissue in the body, is innervated by sensory nerves that control the blink reflex and allow the eye to wash away potential pathogens, allergens, and/or irritants. After infection with HSV-1, corneal sensory nerves retract and are replaced with sympathetic nerves, which lack the ability to sense stimuli. As a result, the infected eye loses the ability to blink, which leaves the ocular surface susceptible to trauma and drying. We hypothesize that this mechanism is largely responsible for the disease associated with HSV-1 infection. Current research in the lab focuses on identifying specific factors regulating sensory nerve retraction and sympathetic nerve growth in hopes of developing novel therapies that preserve blink reflexes.
Grants
National Eye Institute