Abstract

BackgroundThe purpose of the study was to explore the immunological components that are responsible for the proliferative alterations in the different forms of retinal detachment (RD).MethodsVitreous fluids were collected during 23G pars plana vitrectomy from 54 eyes of 54 patients with different RD types, such as rhegmatogenous RD (RRD) without proliferative vitreoretinopathy (PVR) (n = 30), PVR (n = 16) and proliferative diabetic retinopathy (PDR) with tractional RD (n = 8). Vitreous fluids were obtained from 19 eyes with epiretinal membrane (ERM), which were used as control samples. A multiplex chemiluminescent immunoassay was performed to evaluate the concentrations of 48 cytokines, chemokines and growth factors.ResultsThe expression levels of eotaxin, IFN-gamma, IL-6, IL-8, IL-16, MCP-1, MIF and MIP-1 beta were significantly higher in all RD groups than in the ERM group. The levels of CTACK, IP-10, SCGF-beta, and SDF-1 alpha were significantly higher in patients with diabetic tractional RD and PVR than in other patients. The upregulation of VEGF and IL-18 was detected in PDR.ConclusionsOur results indicate that complex and significant immunological mechanisms are associated with the pathogenesis of different forms of RD: selected cytokines, chemokines and growth factors are upregulated in the vitreous of eyes with RD. The detected proteins are present in different concentrations both in RRD and PVR. In the presence of PVR and PDR, the majority of cytokines are upregulated; thus, they may serve as biomarkers to estimate the progression or severity level of proliferation and later to develop personalized therapeutic strategies to slow down or prevent pathological changes.

Highlights

  • The purpose of the study was to explore the immunological components that are responsible for the proliferative alterations in the different forms of retinal detachment (RD)

  • Seven cytokines were upregulated in all RD groups (RRD, proliferative vitreoretinopathy (PVR) and proliferative diabetic retinopathy (PDR)) compared to controls: levels of IL-6 (p < 0.001, p < 0.001 and p < 0.001, respectively), IL-16 (p < 0.01, p < 0.001 and p < 0.001, respectively), IFN-gamma (p < 0.001, p < 0.001 and p < 0.05, respectively), Monocyte chemotactic protein (MCP)-1 (p < 0.001, p < 0.001 and p < 0.01, respectively), and Macrophage migration inhibitory factor (MIF) (p < 0.001, p < 0.001 and p < 0.001, respectively) were significantly higher in all RD groups than in the epiretinal membrane (ERM) group

  • Wladis et al documented that IL4, IL-5, IL-6, IL-15, G-CSF, Granulocytemacrophage colony-stimulating factor (GM-CSF), Interferon gamma–induced protein 10 (IP-10), Macrophage inflammatory protein (MIP)-1 alpha, Stem cell factor (SCF), and SCGF were significantly increased in PVR compared to primary rhegmatogenous RD (RRD) and ERM [15]

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Summary

Introduction

The purpose of the study was to explore the immunological components that are responsible for the proliferative alterations in the different forms of retinal detachment (RD). Retinal detachment (RD) can cause vision loss if untreated, and even with proper surgical intervention, a potentially sight-threatening condition may develop in some cases. PVR is based on the development of fibrocellular membranes on the surface of and under the retina after RRD [1]. PDR is characterized by neovascularization on the retina and the formation of fibrovascular membranes at the vitreoretinal interface. Iyer et al proposed a surgical algorithm for the management of PDR with tractional RD based on their compilation of relevant literature [4]. Because of these difficulties, the pathophysiology of PVR and PDR, including cytokines, chemokines and other inflammatory factors, is under investigation [5]

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