Suppression of Experimental Autoimmune Uveitis in Lewis Rats by Oral Administration of RecombinantEscherichia coliExpressing Retinal S-Antigen

Experimental autoimmune uveitis (EAU) is an organ-specific T-lymphocyte-mediated autoimmune disease which serves as a model for several human ocular inflammations of an apparently autoimmune nature. S-antigen, a photoreceptor cell protein, is highly efficient in inducing EAU showing severe inflammation of the uveal tract and retina of the eye. We have demonstrated previously that recombinantEscherichia coliexpressing retinal S-antigen induces EAU in Lewis rats. The oral administration of S-antigen prior to the uveitopathogenic challenge results in significant suppression of the disease and of the cellular responses. We examined the effect of oral administration ofE. coliexpressing retinal S-antigen on the development of EAU induced with native S-antigen in Lewis rats. Feeding rats with 1 mg of bacteria on Days 7, 5, 3, 2, and 1 prior to immunization with 50 μg of retinal S-antigen caused a significant suppression of the disease. Moderate suppression was found in animals fed 0.5 and 0.25 mg of recombinant bacteria. Oral feeding of 1 mg of JM105 transfected with plasmid alone had no significant effect on the subsequent induction of EAU by S-antigen. Feeding recombinantE. coliexpressing retinal S-antigen before immunization significantly decreased the proliferative response of lymphocytes to native S-antigenin vitro.Our results indicate that recombinant microorganism-expressing autoantigen administered orally induces suppression of specific autoimmune disease as well as cellular response to particular autoantigen.