Background: Multiple sclerosis (MS) is often accompanied by optic nerve inflammation. And some patients experience permanent vision loss. We examined if the grade of optic nerve infiltration and demyelination affects the severity of clinical signs in an experimental autoimmune encephalomyelitis (EAE) model. The loss of retinal ganglion cells (RGC) and alterations in glia activity were also investigated. Methods: C57BL/6 mice were immunized with peptide MOG_35-55 in complete Freund’s adjuvant (CFA) and controls received PBS in CFA. Then 23 days post immunization eyes were prepared for flatmounts and stained with Nissl to evaluated neuronal density. Clinical EAE symptoms as well as cell infiltration and demyelination in the optic nerve were examined. Retinal sections were stained with hematoxylin and eosin and silver stain. Immunohistochemistry was used to label RGCs (Brn-3a), apoptotic cells (caspase 3), macroglia (glial fibrillary acidic protein (GFAP)), microglia (Iba1), macrophages (F 4/80) and interleukin-6 (IL-6) secretion. Results: EAE symptoms started at day 8 and peaked at day 15. Cell infiltrations (P = 0.0047) and demyelination (P = 0.0018) of EAE nerves correlated with the clinical score (r > 0.8). EAE led to a significant loss of RGCs (P< 0.0001). Significantly more caspase 3⁺ cells were noted in these animals (P = 0.0222). They showed an increased expression of GFAP (P< 0.0002) and a higher number of microglial cells (P< 0.0001). Also more macrophages and IL-6 secretion were observed in EAE mice. Conclusions: MOG immunization leads to optic neuritis and RGC loss. EAE severity is related to the severity of optic nerve inflammation and demyelination. EAE not only affects activation of apoptotic signals, but also causes a glial response in the retina.

Purpose: To show the existence of IgG antibodies against retinal antigens in aqueous humor of normal tension glaucoma patients. Methods: Forty-two patients were included in this study. Aqueous humor was collected from control subjects (CO; n = 21) and patients with normal tension glaucoma (NTG; n = 21). Western blot methods against bovine retinal antigens were used to detect the IgG antibody patterns. The complex antibody repertoires were analyzed by multivariate statistical techniques. Mass spectrometry was used to identify the most important antigens. Results: Very complex IgG antibody patterns against retinal antigens were found in all analyzed aqueous humor samples. Our multivariate approach could quantify differences in immunoreactivities, and including all peaks, the analysis of discriminance revealed a statistical significant difference between the patterns of the NTG and the CO group (p < 0.001). The antigen band at 21 kDa was identified as α B-crystallin, the 57-kDa antigen band as vimentin, and one at 70 kDa as heat shock protein 70. Conclusions: We could demonstrate that complex IgG antibody patterns against retina exist in aqueous humor. The significant differences in the antibody pattern of the glaucoma group compared with the nonglaucoma group in aqueous humor confirm the results of previous studies using sera of glaucoma patients. These differences in antibody patterns might be further evidence for an autoimmune involvement in the pathogenesis of some glaucoma patients.

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 E ₂ 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 E ₂ 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 E ₂ level or between corneal incision, suction time, or laser time in the femto groups and prostaglandin/prostaglandin E ₂ 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. [ J Refract Surg. 2013;29(11):742–747.]

Purpose. Glaucoma is characterized by a progressive loss of retinal ganglion cells that results in a characteristic optic neuropathy associated with visual field loss. In previous studies, changes in the antibody profiles have been shown in the sera of patients with glaucoma, and these findings suggest a role for autoimmune involvement in the pathogenesis of glaucoma in some patients. The purpose of this study was to compare the antibody profiles against optic nerve antigens in patients with glaucoma in two different study populations from Germany and the United States.

Purpose. Ischemia is a risk factor for eye diseases like ocular vein occlusion or glaucoma. To investigate effects of ischemia-reperfusion (I/R) a lot of different animal models are used, studying one or two different cell types, which creates heterogeneity of data. The aim of this study was to investigate the function and morphology of the whole retina and different retinal cell types in an I/R model. Methods. I/R was induced by elevating the intraocular pressure in the right eyes of rats. Twenty-one days after ischemia, electroretinogram measurements were performed. Changes in layer thickness were investigated. Changes of RGC, amacrine-, rod bipolar-, and glia cells as well as presence of apoptosis were analyzed immunohistologically. Results. A-wave- and b-wave amplitudes were decreased; histology showed a reduction of RGC- and inner plexiform layer thickness and a 29% loss of RGCs occurred in ischemic eyes (P = 0.016). An increase of apoptotic cells was detected in the GCL and INL of ischemic retinas (P < 0.05). Also, a loss of cholinergic amacrine cells (control: 11 ± 1 cells/mm, I/R: 4 ± 1 cells/mm, P < 0.001), but no change in rod bipolar cell numbers was noted. Conclusions. Our study allowed a comparison of the effects of I/R for different retinal cell types. Cells in the outer retina seemed to be more resistant to ischemic damage compared with cells of the inner retina. We hypothesize that a degenerative process, like a secondary wave of apoptosis, occurs 21 days after I/R, causing progressive damage in the retina.