Early involvement of nitric oxide in mechanisms of pathogenesis of experimental autoimmune uveitis induced by interphotoreceptor retinoid-binding protein (IRBP)

Arroul-Lammali, Amina; Djeraba, Zineb; Belkhelfa, Mourad; Belguendouz, Houda; Hartani, D.; Lahlou-Boukoffa, O.S.; Touil-Boukoffa, Chafia

doi:10.1016/j.jfo.2011.05.003

Cited by 14 publications

(6 citation statements)

References 40 publications

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“…As previously reported by our team, during EAU activity, a signi cant proportion of damages in ocular structures was observed and attributed mainly to nitric oxide (Djeraba et al 2010;Arroul-Lammali et al 2012;Touri et al 2019). In addition, TNF-α, has been shown to be an important cytokine involved in alteration of ocular tissue (Dick et al 2004).…”

Section: Discussionsupporting

confidence: 78%

Beneficial Effect of Dimethyl Fumarate on Experimental Autoimmune Uveitis is Dependent of Pro-Inflammatory Markers Immunomodulation

Touil-Boukoffa

Labsi

Soufli

et al. 2021

Preprint

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Autoimmune uveitis is an inflammatory disease of the eye and is one of the major causes of blindness worldwide. Experimental autoimmune uveoretinitis (EAU) constitutes an animal disease model of human endogenous uveitis. In our study, we investigated the immunomodulatory effect of Dimethylfumarate (DMF) using bovine retinal extract-induced uveitis in a Female Wistar rats. To evaluate the in vivo efficacy, Female Wistar rats were divided into 7 experimental groups: control group (n = 5), consisting of non-immunized animals; Uveoretinitis (n = 5), and DMF/Uveoretinitis groups (n = 15), which received a subcutaneous injection of bovine retinal extract emulsified in complete Freund’s adjuvant; MC group (n = 5), treated by daily intragastric administration of methylcellulose 0.08% in tap water; DMF group, consisting of control positive group, rats received daily oral gavage administration of 500 µL of Dimethylfumarate at 100mg/Kg dissolved in 0.08% methylcellulose in tap water (n = 5). On days 14 post immunization, the rats were then euthanized and associated indications were investigated to evaluate the therapeutic efficacy. Nitric oxide (NO) and TNF-α were assessed in plasma. Meanwhile, eyes were collected for histological and immunohistochemical studies. The retinal expression of iNOS, CD68, CD20, CD25, CD4, and CD8 was examined. Interestingly, DMF enhanced a significant reduction of NO and TNF-α production in the treated group. This effect was strongly related to the histological structure of eyes improvement. In the same context, a significant decrease of iNOS, CD68, and CD20 expression and CD25 increase expression were reported in retinal tissue of DMF/Uveoretinitis group in comparison to the immunized group. Collectively, our results indicate that DMF treatment has a beneficial effect in experimental autoimmune uveoretinitis and could constitute a good candidate for monitoring an ocular inflammatory diseases.

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Section: Discussionsupporting

confidence: 78%

Beneficial Effect of Dimethyl Fumarate on Experimental Autoimmune Uveitis is Dependent of Pro-Inflammatory Markers Immunomodulation

Touil-Boukoffa

Labsi

Soufli

et al. 2021

Preprint

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“…Immunotherapies have also proven to be effective in treating retinal and optic nerve disorders (8-11, 21, 44, 45). One of the self-Ags commonly used for treating eye diseases is IRPB, a classic inducer for EAU models (19,20,25,46). IRBP was found to be effective in protecting RGCs against various injuries such as high intraocular pressure (8), toxicity of intraocular glutamate injection (45), and optic nerve crush (21).…”

Section: Discussionmentioning

confidence: 99%

Photoreceptor IRBP prevents light induced injury

Sun

Meng

Liu³

et al. 2016

Front Biosci

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Interphotoreceptor retinoid-binding protein (IRBP) is a classic inducer of experimental autoimmune uveoretinitis (EAU). Although IRBP causes neuronal loss in susceptible animals, resistant animals such as Sprague-Dawley (SPD) rats can benefit from the evoked protective autoimmune responses. The aim of the present study was to analyze the neuroprotective effects of IRBP against light-induced photoreceptor degeneration. We immunized 75 male SPD rats with IRBP and the rats were then exposed to blue light for 24 hours (IRBP group). Seventy five rats were included in the control group. We found that the number of apoptotic cells in the outer nuclear layer (ONL) peaked on 1 day after light exposure, and the ONL thickness decreased significantly on day 3. OX42-positive cells appeared in the ONL immediately after light exposure, and their number peaked on day 3, and changed from resting ramified cells to activated amoeboid cells. Compared with the control group (n=75), the IRBP group showed less apoptotic cells, a thicker ONL, and reduced expression of tumor necrosis factor-alpha. These outcomes indicate the IRPB might protect retinal photoreceptors against light-induced injury.

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“…Some epitopes of S antigen were found to share homology with particular amino acid regions of HLA-B51 and HLA-B27, which suggests that this antigen contributes to the pathogenesis of BU [ 16 , 17 ]. In addition, retinal tissue damage and significant increase in nitric oxide (NO) production were found in experimental models of autoimmune uveitis induced by S antigen or interphotoreceptor retinoid binding protein [ 18 , 19 ].…”

Section: Antigens and Autoantigens In The Pathogenesis Of Behçet'smentioning

confidence: 99%

Immunopathogenesis of Ocular Behçet’s Disease

Park

Kim

2014

Journal of Immunology Research

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Behçet's disease (BD) is a chronic recurrent systemic inflammatory disorder of unknown etiology characterized by oral and genital ulcerations, skin lesions, and uveitis. The ocular involvement of BD, or Behçet's uveitis (BU), is characterized by panuveitis or posterior uveitis with occlusive retinal vasculitis and tends to be more recurrent and sight threatening than other endogenous autoimmune uveitides, despite aggressive immunosuppression. Although pathogenesis of BD is unclear, researches have revealed that immunological aberrations may be the cornerstone of BD development. General hypothesis of BD pathogenesis is that inflammatory response is initiated by infectious agents or autoantigens in patients with predisposing genetic factors and perpetuated by both innate and acquired immunity. In addition, a network of immune mediators plays a substantial role in the inflammatory cascade. Recently, we found that the immunopathogenesis of BU is distinct from other autoimmune uveitides regarding intraocular effector cell profiles, maturation markers of dendritic cells, and the cytokine/chemokine environment. In addition, accumulating evidence indicates the involvement of Th17 cells in BD and BU. Recent studies on genetics and biologics therapies in refractory BU also support the immunological association with the pathogenesis of BU. In this review, we provide an overview of novel findings regarding the immunopathogenesis of BU.

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Early involvement of nitric oxide in mechanisms of pathogenesis of experimental autoimmune uveitis induced by interphotoreceptor retinoid-binding protein (IRBP)

Cited by 14 publications

References 40 publications

Beneficial Effect of Dimethyl Fumarate on Experimental Autoimmune Uveitis is Dependent of Pro-Inflammatory Markers Immunomodulation

Beneficial Effect of Dimethyl Fumarate on Experimental Autoimmune Uveitis is Dependent of Pro-Inflammatory Markers Immunomodulation

Photoreceptor IRBP prevents light induced injury

Immunopathogenesis of Ocular Behçet’s Disease

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