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Xiaodong Zheng, Masahiko Yamaguchi, Tomoko Goto, Shigeki Okamoto, Yuichi Ohashi; Experimental Corneal Endotheliitis in Rabbit. Invest. Ophthalmol. Vis. Sci. 2000;41(2):377-385.
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© 2016 Association for Research in Vision and Ophthalmology.
purpose. Corneal endotheliitis may cause permanent visual loss due to
endothelial decompensation. The pathogenesis underlying this distinct
clinical entity is not known. In the current study, a rabbit herpetic
corneal endotheliitis model was made of induced anterior
chamber-associated immune deviation (ACAID).
methods. One group of rabbits received left-eye intracameral inoculation of
UV-inactivated herpes simplex virus (HSV)-1 (strain McKrae). The second
group received cell medium in the same manner as the first group. The
third group subcutaneously received the same inoculum as the first
group. Seven days later, all right eyes were intracamerally infected
with 2.5 × 104 plaque-forming units of infectious
HSV-1. Eyes were evaluated by slit lamp examination. Two weeks after
infection, rabbits were killed, and right eyes were examined by
immunohistochemical staining and electron microscopy. Aqueous humor was
detected for HSV-1 DNA and antibody.
results. Nonspecific inflammation occurred in the anterior segments of the eyes
from the second and third groups. In contrast, at 14 days after
infection, the first group of rabbits showed a specific pattern of
inflammation that greatly resembled clinical features of corneal
endotheliitis. Viral antigen was detected only in the endothelial
layer. Electron microscopy revealed enlarged intercellular gaps and
infiltration of inflammatory cells that are characteristic of
endothelial defects. HSV-1 DNA was detected at a significantly higher
number in the aqueous humor aspirates from endotheliitis rabbits. In
addition, ACAID was shown to be induced in the rabbits with corneal
conclusions. HSV-1 infection can induce corneal endotheliitis and ACAID may play the
pivotal role in this entity.
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