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In vivo imaging of retinal inflammation in experimental autoimmune uveoretinitis
Author(s) -
XU H
Publication year - 2009
Publication title -
acta ophthalmologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.534
H-Index - 87
eISSN - 1755-3768
pISSN - 1755-375X
DOI - 10.1111/j.1755-3768.2009.2312.x
Subject(s) - retinal , pathology , medicine , retina , in vivo , preclinical imaging , inflammation , fundus (uterus) , scanning laser ophthalmoscopy , ophthalmology , biology , immunology , neuroscience , microbiology and biotechnology
Abstract Purpose Experimental animal models are essential for us to understand the pathogenesis of human diseases. Posterior uveoretinitis can be modelled in mice with IRBP immunization (i.e. experimental autoimmune uveitis, EAU), whereas a number of mouse models are also available for age‐related macular degeneration (AMD). With the advancement in new technologies, it is now possible to image inflammatory retinal changes in experimental mice in vivo none invasively. The aim of the study is to clinical revisit the traditional retinal inflammation animal models with modern imaging techniques. Methods EAU was induced in C57B/6 mice with IRBP peptide 1‐20. Aged CCL2 knockout mice were used as an AMD model. Retinal inflammatory changes were imaged in vivo non‐invasively using topical endoscopic fundus imaging system and the scanning laser ophthalmoscopy (SLO) system. Results Inflammatory retinal changes in the early stages of EAU were characterised as retinal oedema, vascular sheathing, multiple small retinal infiltrates or large linear retinal infiltrates. “Snow‐ball”‐like vitreous infiltrates were observed in the inferior part of the fundus at the peak stage of EAU. Using SLO autofluorescent (AF)‐macrophages were detected at the peak stages of EAU and were located predominately around inflamed retinal venules. At the late stages of EAU, retinal scars and intraretinal neovascular membranes were observed. In the retina aged CCL2 KO mice, regional retinal atrophy and dursen‐like multiple lesions were observed. Dursen‐like changes were autofluorescent in SLO examination. Ex vivo confocal microscopy indicated that they were not dursen but subretinal lipofuscin‐loaded microglial cells. Conclusion EAU mimics many aspects of human posterior uveoretinitis including retinal vasculitis, multifocal choroiditis. Late stage EAU could be a good model for inflammation induced retinal neovascularisation. CCL2 KO mouse is a model of dry‐AMD.