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Biomedical subjects

R H Meyers-Elliott

Publications and source records attributed to R H Meyers-Elliott.

16 recordsLinked to original sources
PubMed1987

Effect of cyclosporine A on the corneal inflammatory response in herpes simplex virus keratitis.

The effects of cyclosporine A (CyA), a selective inhibitor of T-lymphocyte function, on the corneal inflammatory response in herpes simplex virus (HSV) stromal keratitis was followed during the course of experimental HSV keratitis in the rabbit. The corneal response, characterized by polymorphonuclear leukocytes (PMN) and mononuclear cells, is an immunologically specific event that is dependent on the presence of viral antigens and immune cells. CyA treatment during the course of HSV keratitis resulted in a more severe and persistent stromal disease and more anterior chamber involvement than that seen in the solvent control-treated HSV-infected animals. Clinical observations correlated well with histological studies which confirmed a greater incidence of mononuclear and PMN infiltrates throughout the anterior chamber and stroma in the CyA-treated animals. HSV antigens were present in the corneas from both infected groups as observed by immunofluorescence staining, but endothelial localization of HSV antigens was seen primarily in the CyA-treated animals, often accompanied by cells in the anterior chamber. No significant differences in IgG and IgM staining in the diseased corneas and anterior chamber were noted between the CyA-treated and solvent control groups which suggests that there was no local B-cell immunosuppression.

Animals↗
PubMed1987

Routes of viral spread in the von Szily model of herpes simplex virus retinopathy.

Intraocular inoculation of herpes simplex virus type 1 (HSV-1) in one eye of rabbits results in encephalitis and contralateral necrotizing viral retinopathy. The effects of viral inoculation site and optic nerve (ON) transection on the spread of virus to the brain and contralateral eye in this model were investigated. A surgical technique was developed for transection of the retrobulbar optic nerve posterior to the entrance of the central retinal vessels. HSV-1 was inoculated into the AC or vitreous of one eye in normal rabbits and in rabbits with one ON transected, either ipsilateral or contralateral to the side of inoculation. Animals were followed clinically for signs of disease. Encephalitis and contralateral retinopathy (CR) occurred following both AC and vitreous inoculation of virus, although CR developed later in AC-inoculated rabbits. Ipsilateral retinopathy (IR) developed in 83% of vitreous-inoculated rabbits, but in only 5% of AC-inoculated animals. IR developed 8 days after the onset of CR in the AC-inoculated group. ON transection on the side of virus inoculation prevented development of CR only in vitreous-inoculated rabbits. ON transection on the side opposite virus inoculation prevented CR regardless of the site of inoculation. These findings suggest that HSV-1 can leave the inoculated eye by multiple routes depending on the site of virus inoculation, but that virus reaches the retina of the contralateral eye via the optic nerve.

Animals↗
PubMed1987

Effects of cyclosporine A on clinical and immunological parameters in herpes simplex keratitis.

The immunosuppressive effects of cyclosporine A (CyA) on the clinical and antiviral immune responses were examined in experimental herpes simplex virus (HSV) keratitis in the rabbit in order to clarify the role that immune lymphocytes play in herpetic stromal disease. Cyclosporine A was administered intramuscularly to rabbits daily starting from the time of corneal infection with HSV until day 14 postinfection. Control HSV-infected rabbits received daily injections of the solvent vehicle alone. HSV-infected rabbits receiving CyA treatment showed more severe and persistent stromal keratitis, and a greater incidence and duration of virus recovery from the cornea. Suppression of cellular immune responses to T cell mitogens, B cell mitogens (anti-rabbit immunoglobulins), and HSV antigens were observed in the CyA treatment group. These results show that in CyA-treated HSV-infected rabbits the antiviral immune responses are inhibited. Acute viral infections with cytopathic viruses such as HSV may therefore be more dramatic, suggesting that CyA may facilitate the potentiation of HSV infections ordinarily suppressed by immune cells.

Animals↗
PubMed1985

Autoimmunity in hereditary retinal degeneration. I. Basic studies.

One hundred and sixteen patients with retinitis pigmentosa (RP), 64 patients with other eye diseases, and 36 control subjects with no known eye disease were examined for antiretinal autoimmune activity. Sera were screened by indirect immunofluorescence on normal donor human eye sections to detect antibodies to human retinal antigens. Forty three of 116 RP patients (37%), 21 out of 64 non-RP patients with other eye diseases (33%), and 1 out of 42 controls (2%) had antibodies reacting with donor eye retinal antigens. Lymphocytes were tested by an in vitro transformation assay to detect cell mediated immunity to retinal antigens. Sixteen RP patients (19%), 11 non-RP patients (18%), and four controls (10%) showed lymphocyte sensitisation. Autoimmune responses were detected in many degenerative ocular disorders, but it is not known if they play a contributory pathogenic role.

Autoantibodies↗
PubMed1985

Autoimmunity in hereditary retinal degenerations. II. Clinical studies: antiretinal antibodies and fluorescein angiogram findings.

Testing by indirect immunofluorescence for the detection of antiretinal antibodies and lymphocyte stimulation for cell-mediated immunity to retinal antigens was performed on blood obtained from 59 patients with retinitis pigmentosa (RP) and 29 without RP who had other types of retinal disease. The results from the patients' immunological studies were correlated in a masked fashion with six parameters of the fluorescein angiogram: disc staining, peripapillary oedema, vascular arcade oedema, macular oedema, and focal vascular staining (late phases), and disc telangiectasia (early phases). Significant correlations for both groups together were found for IgG antiretinal antibody reactivity and macular oedema (p less than 0.038) and disc staining (p less than 0.033). The non-RP retinal disease group had more significant correlations, including IgG antiretinal antibody reactivity with vascular arcade oedema (p less than 0.018), disc staining (p less than 0.018), and peripapillary oedema (p less than 0.023); the RP patients had significant correlation with IgG reactivity and arcade oedema (p less than 0.045). With combinations of IgG, IgM, and lymphocyte reactivity various significant correlations were found with the fluorescein angiogram.

Adult↗
PubMed1983

Experimental retinal autoimmunity (ERA) in strain 13 guinea pigs: induction of ERA-retinopathy with rhodopsin.

Strain 13 guinea pigs injected with either homologous or bovine rhodopsin, the visual pigment of the retinal outer segments, in complete Freund's adjuvant (CFA) developed experimental retinal autoimmunity (ERA). Initial clinical signs of disease were seen within 21 days after immunization. Pathologic examination of the eyes revealed the presence of inflammatory cells in the choroid and the destruction of the retinal rod outer segments. The unique feature of this disease is that despite the destruction of the inner and outer segments of the retina, at no time is there a substantial inflammatory cell infiltrate. Even as late as 45 days after immunization, when destruction of the retinal ganglion cell layer was noted, no inflammatory cells were detected in the retina. These findings suggest that the retinal inner and outer segments are the target of the autoimmune reaction subsequent to sensitization with purified rhodopsin-CFA.

Animals↗
PubMed1983

Localization of specific autoantibodies in the retinal photoreceptor cell layer in experimental retinal autoimmunity.

The presence and localization of autoantibodies was determined in strain 13 guinea pigs with experimental retinal autoimmunity (ERA) induced by immunization with rhodopsin and rod outer segments (ROS). Sera were obtained from rhodopsin-immunized and from ROS-immunized guinea pigs before, during, and after onset of clinical uveitis. Autoantibodies were detected by indirect immunofluorescent staining of autogenic retinas as well as normal guinea pig retinas. Sera from animals with clinical disease showed specific labeling of the photoreceptor cell layer of the retina. The rhodopsin autoantibody showed a more defined specificity than the ROS autoantibody staining, only the retinal photoreceptors and retinal pigment epithelium. Specific fluorescence was localized only in the retina, and not in any other ocular or nonocular tissues. Neither the rhodopsin nor the ROS antibodies stained the uvea. Sera from animals taken before the onset of clinical disease did not demonstrate the presence of retinal-binding autoantibodies. These findings suggest that photoreceptor-binding autoantibodies appear in the sera of animals immunized with rhodopsin and with ROS, but only in animals with clinical disease. However, these antibodies probably are not the primary cause of pathology, since previous passive transfer experiments (data not shown here) could not be achieved with anti-ROS or with anti-rhodopsin antibodies. These autoantibodies could occur secondarily as a response to the bovine antigens which cross-reacted with the autologous guinea pig antigens. Subsequently these antibodies could be of primary importance in further tissue alteration and destruction.

Animals↗
PubMed1983

Experimental herpesvirus keratitis in the rabbit: topical versus intrastromal infection routes.

Intrastromal and topical routes of infection of rabbit corneas with the HF strain of herpes simplex virus type 1 were compared clinically to determine which route of infection would present the best model of disciform edema and of deep stromal keratitis for our further studies on how the immune response of the infected animals may influence the expression of clinical disease. In addition, virus clearing and persistence of viral antigens as immunologic stimuli were monitored by virologic and electron microscopic immunocytochemical studies. We found topical infection to be preferable to the intrastromal infection route for presenting stromal disease in that it resulted in a higher incidence of epithelial disease with less anterior chamber involvement. The topical infection route model should be valuable in studies of cell-mediated immune response against HSV-infected cells.

Animals↗
PubMed1982

Experimental Klebsiella-induced endophthalmitis in the rabbit.

Klebsiella organisms have been reported in postoperative endophthalmitis. We describe an experimental model of endophthalmitis with anterior segment inflammation over the injection of Klebsiella oxytoca into the rabbit vitreous. Within 24 hours, polymorphonuclear leukocytes were found at the corneal limbus, adjacent to the endothelium, in the iris and ciliary body, throughout the vitreous, and in the optic nerve. Retinal photoreceptor degeneration was widespread within 48 hours. Mononuclear cells appeared in the vitreous within 72 hours. Increased pathologic manifestations concomitant with decreased numbers of recoverable, viable organisms implicate the endotoxins of K oxytoca in the observed pathologic condition. Our model may be useful in further studies on antibiotic therapy in Klebsiella ocular infections and in continuing work on the cross-reaction between Klebsiella and HLA-B27.

Animals↗
PubMed1981

Humoral and cell-mediated immune responses to epidermal growth factor in the rabbit.

Epidermal growth factor (EGF), which has been shown to stimulate epidermal proliferation and keratinization and to induce regeneration of rabbit corneal epithelium, was studied for its immunogenic potential in rabbits. Mouse-derived EGF was administered topically, subconjunctivally, intrastromally, and systemically. Systemic immunization was done both with and without complete Freund's adjuvant (CFA). EGF-stimulated cultures of lymphocytes from peripheral blood, spleen, and lymph nodes of all immunized animals were tested for cell-mediated immunity (CMI) to EGF. All experimental animals demonstrated CMI as determined by either classic positive delayed skin tests or by in vitro production of migration inhibitory factors, regardless of the route of sensitization. Only animals immunized systemically with EGF and CFA produced high-titered specific anti-EGF antibody, and only this group showed ocular reactions after subsequent topical challenge of EGF. These results suggest that antibody to EGF is the major cause for ocular inflammatory reactions observed subsequent to topical EGF challenge of a sensitized animal.

Administration, Topical↗
PubMed1981

Immunopathogenesis of corneal inflammation in herpes simplex virus stromal keratitis: role of the polymorphonuclear leukocyte.

The present studies suggest that polymorphonuclear leukocytes (PMNs) play an essential role in the development of corneal infiltrates in stromal herpes virus (HSV) keratitis. Corneal infiltration was seen rarely in herpes-infected animals treated with anti-PMN serum or with chemotherapy to reduce the numbers of circulating PMNs. By contrast, at least two thirds of the control animals with intact PMNs and infected with herpes virus developed stromal infiltrates. Host complement was localized with HSV antigen and rabbit gamma globulin along with inflammatory cells in the corneas of animals with stromal infiltrates. In the absence of PMN infiltrates, neither complement nor a significant amount of gamma globulin was localized in the corneal stroma. In the PMN-depleted animals, only viral antigen was detected in the stromal keratocytes.

Animals↗
PubMed1980

Viral antigens in the immune ring of Herpes simplex stromal keratitis.

Corneal tissue obtained during superficial keratectomy from a patient with herpesvirus disciform keratitis was studied by immunoelectron microscopy. Clinically, this cornea had a dense central infiltrate with a circumferential opaque ring histologically resembling the immune ring described by Wessely. Histologically, along the line of altered keratocytes and ground substance, an infiltration of inflammatory cells was found. Herpesvirus particles were seen by electron microscopy in the corneal stroma, but these virus particles had abnormal, noninfective forms such as empty capsids and incomplete virions. By immunoelectron microscopy with a peroxidase-labeled antiherpesvirus antibody reagent, herpes-virus antigens were localized inthe corneal keratocytes and in the corneal stroma. The major localization of the virus antigens was in association with the herpes virions and surrounding vacuoles in the keratocyte nucleus and in the corneal stroma in the area of degenerating keratocytes. These findings support the view of a hypersensitivity mechanism in the pathogenesis of herpes simplex virus disciform keratitis.

Antigens, Viral↗
PubMed1980

HLA antigens in recurrent stromal herpes simplex virus keratitis.

HLA-A, HLA-B, and HLA-C antigens were typed on 48 patients with recurrent herpes stromal keratitis. The HLA-Aw30 antigen occurred three times more frequently in patients with herpes stromal keratitis than in those who lack the Aw30 antigen. When the data for the probability of the HLA-Aw30 were corrected for the number of variables studied, the corrected P value was not significant. A previous report of an increased frequency of HLA-B5 with recurrent herpes keratitis was not confirmed by our study. No significant associations with the HLA-C antigens were noted. HLA-DR antigen typing of 25 herpes stromal keratitis patients indicated that the HLA-DRw3 antigen appeared to have an increased frequency in herpes stromal keratitis. However, the small sample size studied precluded interpretation of the increased phenotypic frequency and the possible association of HLA-DRw3 and herpes stromal keratitis needs further study.

HLA Antigens↗
PubMed1980

Induction of cell-mediated immunity in herpes simplex virus keratitis. Kinetics of lymphocyte transformation and the effect of antiviral antibody.

The in vitro lymphoproliferative responses to herpes simplex virus (HSV) antigens were followed in rabbits with herpesvirus infection of the cornea. The proliferative cellular responses occurred early in infection and were demonstrated by lymphoid cells from the local lymph nodes at day 5, the peripheral blood at day 11, and the spleen after day 14. The presence of autologous serum antibodies suppressed lymphoproliferative responses of the lymph node lymphocytes to HSV antigens early in infection at day 5, the time at which antibody production is first noted. Peripheral blood and spleen cells were not appreciably influenced at early time periods. However at 7 months after infection, the presence of autologous serum antibodies stimulated spleen lymphocytes from animals with recurrent disease. These results indicate that antiviral antibodies can affect the cellular immune response in herpesvirus infections by modulating the lymphoproliferative response to herpes antigens.

Animals↗