The role of innate immune system mediators in the development of retinal neurodegeneration in type 2 diabetes mellitus

Abstract

Purpose. To detect the levels of transform growth factors-β (TGF- β1, TGF- β2, TGF- β3), interferon-ʏ (INF- ʏ), matrix metalloproteinase-9 (MMP-9) and S100B protein in blood serum of patients with type 2 diabetes mellitus (DM) and to reveal the connection of these factors with neurodegenerative changes in the retina. Material and methods. 30 patients, averagely aged 60.3, with type 2 DM and no signs of diabetic retinopathy (DR) (the main group) and 30 healthy individuals (control group) were examined using microperimetry and optical coherence tomography. A sandwich variance estimator of solid phase enzyme-linked immunosorbent assay was used to determine the levels of TGF- β 1, TGF- β2, TGF- β3, INF- ʏ, ММР-9 and S100B protein in blood serum of the subjects examined. Results. The patients with type 2 DM were found to experience an increased level of focal loss of retinal ganglion cells and a drop in the average photosensitivity of the retina. The main group also showed a reliable increase in the level of S100B protein and in the serum level of MMP-9 against the control, but no significant difference between the groups was found in the level of TIMP-1. The level of TGF- β2 was significantly higher in the main group, which also showed a deficiency of TGF- β3. No significant difference was found between the two groups in the levels of TGF- β1 or INF- ʏ. In contrast, a positive correlation was revealed between the levels of S100B, MMP-9 and the volume of focal loss of retinal ganglion cells. Conclusion. Patients with type 2 DM and signs of neurodegeneration of the retina reveal a higher activity of some cytokines and MMP-9. This may indicate an important role of neuroinflammation and dysfunction of the immune system in the retinal neurodegeneration process of DM patients. Further research of other cytokins is required to determine early and more sensitive markers of retinal neurodegeneration.