Phone: (251) 460-6250
FAX: (251) 460-7931
Dr. Robert N. Lausch, Professor Emeritus, received his Ph.D. in Microbiology from the University of Florida in 1966. His postdoctoral training was done at Baylor University College of Medicine. Dr. Lausch has been active on various national boards including Visual Sciences,a Study Section which reviews grant applications for N.I.H. He also serves as an ad hoc reviewer for leading journals in immunology and ophthalmology.
We have been studying the host immune response to herpes simplex virus, a common human pathogen which can cause infection in the eye and various other parts of the body. Herpesvirus ocular infections can result in a sight threatening disease called herpes stromal keratitis (HSK). In this disease the host's efforts to eradicate the virus are so exuberant that the accumulation and activity of inflammatory cells can seriously damage sensitive corneal tissue leading to scar formation and possible blindness. It is known that injured cells release intercellular messengers called cytokines and chemokines which attract white blood cells to sites of infection and activate the migrating cells to clear the virus from infected corneal tissue. Studies are in progress to identify the critical participants and events that comprise the ocular inflammatory response.
A second line of investigation in our laboratory is to search for reagents which can suppress an exuberant ocular inflammatory response. It is known that while certain cytokines promote inflammation other cytokines seem to be able to inhibit this response. We have shown that interleukin 10, a immunoregulatory cytokine, could significantly protect against the development of HSK. Such treatment did not interfere with the capacity of the host to clear the virus from infected ocular tissues. These exciting results suggest that a naturally occurring cytokine may be useful in treating destructive inflammatory disease. Further experiments are being directed toward learning how regulating cytokines exert their protective effect.
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