ovalbumin and Endophthalmitis

Since immune privilege is believed to exist in the eye in order to suppress sight-destroying inflammation, we wondered whether eyes with intraocular inflammation retain the immune privileged state. Intraocular inflammation was induced by injection of lipopolysaccharide (LPS) into the vitreous cavity of BALB/c mouse eyes, which showed a peak in intensity at approximately 9 h. At this time point, inflamed eyes were examined for their capacity to afford immune privilege to injected allogeneic tumor cells, and to promote anterior chamber-associated immune deviation (ACAID) to antigens injected locally. In addition, aqueous humor (AqH) harvested from inflamed eyes was tested for its ability to suppress T cell activation. Surprisingly, eyes with acute, intense intraocular inflammation allowed allogeneic tumor cells to form progressively growing tumors, and these same eyes promoted ACAID. Moreover, AqH harvested from inflamed eyes strongly inhibited T cell activation. We conclude that the type of extreme, intraocular inflammation evoked by intravitreally injected LPS fails to abolish immune privilege in the eye. These findings are discussed in light of the effects of other types of inflammation on the integrity of ocular immune privilege, and with respect to the capacity of the eye to maintain immune privilege by more than one mechanism.

Topics: Animals; Anterior Chamber; Aqueous Humor; Endophthalmitis; Immune Tolerance; Interleukin-6; Lipopolysaccharides; Lymphocyte Activation; Mice; Mice, Inbred BALB C; Mice, Inbred DBA; Ovalbumin; Spleen; T-Lymphocytes

The experiments described were undertaken to determine which cells of guinea pigs immunized by different ocular routes produce the IgG1 and IgG2 antibodies detected in the serum. Guinea pigs were immunized intravitreally, topically, or by intravitreal immunization followed by topical conjunctival challenge. An indirect plaque assay was used to detect antibody producing cells in the cervical lymph nodes and ocular tissues. Passive hemagglutination, passive cutaneous anaphylaxis and ELISA assays were used to detect serum antibody. Both the topical and intravitreal methods initiated a primary antibody response. The guinea pigs developed IgG1 and IgG2 serum antibodies, but IgE and IgA antibodies were not detected. IgG1 and IgG2 plaque forming cells (PFC) were found in the lymph node and uveal tissues of the intravitreally immunized guinea pigs, and in the lymph node and conjunctival tissues of the topically immunized animals. IgA plaque forming cells were not detected in topically immunized animals. No antibody producing cells were found in intravitreally immunized guinea pigs sacrificed after the first conjunctival challenge (two months after sensitization). The highest numbers of lymph node and conjunctival PFC were found in the animals sacrificed three days after the second or third topical challenge. The numbers of IgG1 antibody producing cells in this group of guinea pigs were usually higher than the numbers of IgG2 PFC. Serum antibody levels, undetectable before challenge, increased after the second challenge. We conclude that both lymph node and ocular cells produce antibody in guinea pigs immunized by ocular routes.

Topics: Animals; Antibodies, Anti-Idiotypic; Antibody-Producing Cells; Conjunctiva; Endophthalmitis; Enzyme-Linked Immunosorbent Assay; Eye; Guinea Pigs; Immunization; Immunoglobulins; Lymph Nodes; Male; Ovalbumin; Uvea