Abstract
Glaucoma causes blindness due to the progressive death of retinal ganglion cells. The immune response chronically and subclinically mediates a homeostatic role. In current clinical practice, it is impossible to analyse neuroinflammation non-invasively. However, analysis of vitreous images using optical coherence tomography detects the immune response as hyperreflective opacities. This study monitors vitreous parainflammation in two animal models of glaucoma, comparing both healthy controls and sexes over six months. Computational analysis characterizes in vivo the hyperreflective opacities, identified histologically as hyalocyte-like Iba-1+ (microglial marker) cells. Glaucomatous eyes showed greater intensity and number of vitreous opacities as well as dynamic fluctuations in the percentage of activated cells (50–250 microns2) vs. non-activated cells (10–50 microns2), isolated cells (10 microns2) and complexes (>250 microns2). Smaller opacities (isolated cells) showed the highest mean intensity (intracellular machinery), were the most rounded at earlier stages (recruitment) and showed the greatest change in orientation (motility). Study of vitreous parainflammation could be a biomarker of glaucoma onset and progression.
Highlights
Chronic glaucoma is the leading cause of irreversible blindness in the developed world [1]
Images of the vitreoretinal interface were obtained, using optical coherence tomography (OCT) (HR-OCT Spectralis, Heidelberg® Engineering, Germany), in previous interventional studies carried out by our research group detailing the methodology used for the generation of two different animal models of chronic glaucoma (MEPI and Ms) [50]
The widely used Morrison model [11] was generated with sclerosing injections of episcleral veins (MEPI) of the right eye of Long–Evans rats, performed biweekly for 6 months
Summary
Chronic glaucoma is the leading cause of irreversible blindness in the developed world [1]. Increased intraocular pressure (IOP) is the modifiable risk factor most strongly associated with the onset and progression of the disease [2]. This pathology causes progressive retinal ganglion cell (RGC) death, resulting in irreversible visual field impairment [3,4]. Campimetric alteration is detected when 25–30% of RGCs have died, leading to late diagnosis. With the aim of better understanding the pathogenesis of glaucoma, different models of ocular hypertension have been developed in animals, either by genetic engineering [5,6], or by injection of neurotoxic substances [7,8], or by increasing IOP using pre- and post-trabecular mechanisms [9–11]. There is a known progression in glaucoma of neurodegeneration not dependent on IOP, which has been related to cellular and humoral immune-mediated response [12–15]
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