Abstract
Purpose :
Recent findings from our lab showed upregulation of myeloid-related inflammatory S100A9 protein in human DR patients and DR mice models. However, we have yet to determine the source of S100A9 in the retina. Retinal microglial cells are resident macrophages and have critical functions during retinal injury. Therefore, we hypothesize that retinal microglia under oxidative stress will activate the innate immune response to produce S100A9 protein and inflammatory cytokines in DR.
Methods :
The primary retinal microglial cells (pMic) were cultured from domestic pig eye globes obtained from the local abattoir and treated with LPS (5ng/ml, 25ng/ml, 50ng/ml and 100ng/ml) in the presence and absence of 50mg of minocycline. Immunocytochemistry was performed to characterize the pMic. Cells were positive for Iba1, and negative for glial cell markers - GS and GFAP. Real-time PCR was performed to determine the expression of S100A9 and inflammatory markers (IL-6 and IL-8).
Results :
LPS treatment resulted in a significant increase in IL-6, IL-8 and S100A9 in a dose-dependent manner, which was attenuated by minocycline, an inhibitor of immune and glial activation.
Conclusions :
This is the first study to describe myeloid-related S100A9 production from activated microglia.
This is a 2020 ARVO Annual Meeting abstract.