Abstract

The purpose of this study was to investigate inflammatory cells in vitreous from patients with proliferative diabetic retinopathy (PDR) using flow cytometric analysis. Twenty-eight patients with PDR requiring vitrectomy because of macular traction or tractional retinal detachment were enrolled in the study (n = 28), and 6 patients with macular hole (MH) formed the control group. Samples of vitreous and peripheral venous blood were obtained at the beginning of vitrectomy. T lymphocytes were found in vitreous from patients with PDR, and CD4/CD8 ratio was higher in vitreous (median 4.3) compared to blood (median 1.9; P = 0.003). No B lymphocytes were detected in vitreous. The percentage of histiocytes/macrophages was significantly higher in vitreous (median 62.1) in comparison with blood (median 5.5; P < 0.0001). No lymphocytes were detected in vitreous of the control group. There were more T lymphocytes in vitreous from patients with active PDR. No association between cells in the vitreous and visual acuity improvement after surgery was found. In conclusion, T lymphocytes are found in vitreous from patients with PDR and reflect the activity of PDR but do not seem to predict visual prognosis. Higher CD4/CD8 ratio in vitreous compared to blood from patients with PDR is consistent with local inflammatory response in PDR.

Highlights

  • Diabetic retinopathy (DR) is a late microvascular complication of diabetes mellitus and a leading cause of blindness in the working age population

  • In the control group (MH group) no erythrocytes were found; these samples were considered uncontaminated with blood

  • T lymphocytes were found in most vitreous samples from patients with proliferative diabetic retinopathy (PDR), and CD4/CD8 ratio was higher in vitreous samples in comparison with peripheral blood

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Summary

Introduction

Diabetic retinopathy (DR) is a late microvascular complication of diabetes mellitus and a leading cause of blindness in the working age population. Typical risk factors of DR include hyperglycemia, hypertension, and hyperlipidemia. These factors have been shown to induce retinal inflammation by a variety of mechanisms [1]. There is general acceptance that DR is a low-grade chronic inflammation [2]. Inflammation is a nonspecific response to injury. Many molecular mediators and functional changes with immune cell and resident macrophage activation are involved in the inflammatory response. Leukocytes’ prolonged secretion of inflammatory mediators and toxic oxygen radicals in persisting, chronic inflammation can lead to tissue damage [3, 4]

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