George E. Marak

Patterns of Experimental Allergic Uveitis Induced by Rhodopsin and Retinal Rod Outer Segments

We have observed that both washed outer segments and purified rhodopsin produce primarily a posterior uveitis with little or no anterior segment inflammation if an effort is made to remove all contaminating soluble retinal antigen. The differences in the immunopathologic responses to rhodopsin compared to soluble retinal antigen may be explained by the solubility difference between these antigens. With the soluble retinal antigen there may be anterior segment inflammation and diffuse tissue necrosis. The allergic response to rhodopsin appears to be confined to the posterior segment with tissue necrosis in severe cases restricted to the anatomic distribution of rhodopsin in the outer retina.

Ultrastructural Analysis of Experimental Allergic Uveitis in Rabbit

Bilateral posterior uveo-retinitis was induced in 6 pigmented rabbits by unilateral subconjunctival injection of 50 micrograms of retinal soluble antigen (S-antigen) in complete Freunds adjuvant. Ultrastructurally the inflammation revealed four distinct phases of target cell destruction in the retina. Initially there was a coagulative necrosis of the outer segments of the photoreceptor cells, followed by phagocytosis of these outer segments by mononuclear cells. Next, there was hydropic degeneration and necrosis of the inner segments and the cell bodies, and finally there was proliferation of the retinal pigment epithelium and enlargement of the Müller cells to replace the necrotic photoreceptors. The localized damage to the photoreceptor cells indicates that these cells are the target site in the inflammation induced by S-antigen.

Effects of Mydriatic Agents on Neutrophil Migration

We have investigated the effects of various mydriatic agents on the locomotion of polymorphonuclear leukocytes in vitro. Human as well as rat neutrophils showed a dose-dependent increase of migration into micropore filters when tested against cyclopentolate hydrochloride at a dose range between 16 and 63 micrograms/ml. At higher doses (250 micrograms/ml), a complete inhibition of neutrophil migration was observed. A commercially available cyclopentolate hydrochloride preparation showed identical effects. Little or no changes in neutrophil locomotion were seen with atropine, homatropine, scopolamine or tropicamide when tested at the same concentration range. Since addition of cyclopentolate to either the lower or upper compartment of the multiwell chemotaxis chamber gave virtually the same results, it is assumed that the drug most likely induces a chemokinetic neutrophil response. However, an additional chemotactic effect cannot be excluded. These in vitro observations may help to explain an accidental observation in a patient with severe anterior uveitis who showed a massive, localized leukocyte accumulation on the corneal endothelium after contact with a cyclopentolate-soaked cotton pledget.