Cytokine profiling reveals increased serum inflammatory cytokines in idiopathic choroidal neovascularization

Abstract

Background: The exact pathogenesis of idiopathic choroidal neovascularization (ICNV) remains unclear. Cytokine-mediated inflammation has been thought to be involved in the pathophysiology of ICNV. The purpose of this study was to investigate serum cytokine profiles in patients with ICNV and to explore the relationship between serum cytokine levels and ICNV severity. Methods: This case-control study was conducted in 32 ICNV patients and 30 healthy volunteers. Clinical and demographic information was obtained from the medical data platform and the serum was analysed with a multiplex assay to determine the levels of seven cytokines: interleukin (IL)-2, IL-10, IL-15, IL-17, basic fibroblast growth factor (basic FGF), granulocyte-macrophage colony-stimulating factor (GM-CSF), and vascular endothelial growth factor (VEGF). Results: Serum levels of IL-2, IL-10, IL-17, basic FGF, and VEGF were elevated in ICNV patients compared to controls. Serum GM-CSF levels were positively related to central retinal thickness, and serum IL-17 levels were positively related to CNV lesion area. Conclusion: Serum inflammatory cytokines were significantly elevated in ICNV patients compared to controls. This suggests that systemic inflammation may play a critical role in the physiopathology of ICNV.

Efficacy and Safety of Aflibercept for the Treatment of Idiopathic Choroidal Neovascularization in Young Patients

“…However, we cannot rule out the possibility that some patients might have had a silent underlying inflammation or other conditions associated with the development of CNV. 34,35 Another limitation is the absence of a control group, showing the natural evolution of iCNV without treatment. However, at the time of patient inclusion, no comparative active treatments were approved.…”

Cytokine Profiles and the Effect of Intravitreal Aflibercept Treatment on Experimental Choroidal Neovascularization

“…GM-CSF drives the proliferation of many myeloid cell types, such as granulocytes, macrophages, and monocytes [28]. Previous reports have shown that GM-CSF is significantly elevated in the aqueous humor of CNV patients [6]. Immune/inflammation reaction occurs at this stage of CNV formation.…”

“…Although vascular endothelial growth factor (VEGF) is known as a potent proangiogenic factor [4], the exact pathogenesis of CNV is complex and has not been fully elucidated. Accumulating evidence has demonstrated inflammation to play an important role in the pathogenesis of CNV [5,6]. Guo et al [6] reported that serum inflammatory cytokines are significantly elevated and involved in idiopathic CNV patients.…”

“…Accumulating evidence has demonstrated inflammation to play an important role in the pathogenesis of CNV [5,6]. Guo et al [6] reported that serum inflammatory cytokines are significantly elevated and involved in idiopathic CNV patients. Nagineni et al [7] reported that interferon-γ, tumor necrosis factor (TNF)-α, and interleukin (IL)-1 could enhance the secretion of VEGF, given that inflammatory cytokines are associated with CNV formation.…”