Elevated Glucose and Interleukin-1 β Differentially Affect Retinal Microglial Cell Proliferation.

Diabetic retinopathy is considered a neurovascular disorder, hyperglycemia being considered the main risk factor for this pathology. Diabetic retinopathy also presents features of a low-grade chronic inflammatory disease, including increased levels of cytokines in the retina, such as interleukin-1 beta (IL-1 beta). However, how high glucose and IL-1 beta affect the different retinal cell types remains to be clarified. In retinal neural cell cultures, we found that IL-1 beta and IL-1RI are present in microglia, macroglia, and neurons. Exposure of retinal neural cell cultures to high glucose upregulated both mRNA and protein levels of IL-1 beta. High glucose decreased microglial and macroglial cell proliferation, whereas IL-1 beta increased their proliferation. Interestingly, under high glucose condition, although the number of microglial cells decreased, they showed a less ramified morphology, suggesting a more activated state, as supported by the upregulation of the levels of ED-1, a marker of microglia activation. In conclusion, IL-1 beta might play a key role in diabetic retinopathy, affecting microglial and macroglial cells and ultimately contributing to neural changes observed in diabetic patients. Particularly, since IL-1 beta has an important role in retinal microglia activation and proliferation under diabetes, limiting IL-1 beta-triggered inflammatory processes may provide a new therapeutic strategy to prevent the progression of diabetic retinopathy.