Immune response against ocular tissues after immunization with optic nerve antigens in a model of autoimmune glaucoma.

PURPOSE: In recent years, numerous studies have investigated the involvement of immunological mechanisms in glaucoma. Until now, it has not been determined whether the altered antibody pattern detected in patients is harmful to retinal ganglion cells (RGCs) or triggers disease formation in any way. In a model of experimental autoimmune glaucoma, RGC loss can be induced through immunization with certain ocular antigens. In the current study, the time course of the levels of autoreactivity against ocular tissues after immunization was examined. METHODS: Intraocular pressure was measured regularly. Ten weeks after immunization with an optic nerve homogenate antigen (ONA), the number of RGCs was determined. Immunoglobulin G levels in aqueous humor were measured via enzyme-linked immunosorbent assay at the same time point. Serum from different time points was used to analyze the possible occurrence of autoreactive antibodies against the retina or optic nerve in this autoimmune glaucoma model. Additionally, optic nerve and brain sections were evaluated for possible pathological findings. RESULTS: Intraocular pressure stayed within the normal range throughout this study. A continuous increase of autoreactive antibodies against the optic nerve and retina sections was observed. At 4, 6, and 10 weeks, antibody reactivity was significantly higher in ONA animals (p<0.01). Aqueous humor immunoglobulin G levels were also significantly higher in the ONA group (p=0.006). Ten weeks after immunization, significantly fewer RGCs were noted in the ONA group (p=0.00003). The optic nerves from ONA animals exhibited damaged axons. No pathological findings appeared in any brain sections. CONCLUSIONS: Our findings suggest that these modified antibodies play a substantial role in mechanisms leading to RGC death. The slow dissolution of RGCs observed in animals with autoimmune glaucoma is comparable to the slow progressive RGC loss in glaucoma patients, thus making this a useful model to develop neuroprotective therapies in the future.

Changes in prostaglandin levels in patients undergoing femtosecond laser-assisted cataract surgery.

PURPOSE: To investigate the intraocular prostaglandin concentrations after femtosecond laser treatment and the potential relationship to miosis. METHODS: Aqueous humor was collected from patients after femtosecond laser pretreatment and at the beginning of routine cataract surgery. The total prostaglandin and the prostaglandin E2 concentrations were measured in two independent studies using an enzyme-linked immunoassay. RESULTS: A significantly higher level of prostaglandins was noted in the aqueous humor of patients immediately after femtosecond laser treatment. This could be confirmed in two studies consisting of independent patient populations (study I: control = 17.3 ± 4.0 pg/mL [n = 22], femtosecond laser [femto] = 182.1 ± 38.1 pg/mL [n = 22], P = .0001, and study II: control = 17.5 ± 1.4 pg/mL [n = 37], femto: 377.1 ± 83.6 pg/ mL [n = 35], P = .00004). A significant increase of prostaglandin E2 was noted in two measurements (study III: control = 4.5 ± 1.9 pg/mL [n = 13], femto: 19.2 ± 2.5 pg/mL [n = 20], P = .0002, and study IV: control = 11.3 ± 1.6 pg/mL [n = 35], femto: 60.3 ± 16.1 pg/mL [n = 36], P = .004). No correlation was noted between age or cataract density and prostaglandin/prostaglandin E2 level or between corneal incision, suction time, or laser time in the femto groups and prostaglandin/prostaglandin E2 level. CONCLUSIONS: Prostaglandins rise immediately after femtosecond laser treatment. Future patients should perhaps be treated with non-steroidal anti-inflammatory drugs to maintain mydriasis before undergoing femto-second laser treatment for cataract surgery.