Neuroinflammation plays a vital role in the process of a variety of retinal ganglion cells (RGCs) degenerative diseases including
traumatic optic neuropathy (TON).
Retinal microglial activation is believed as a harbinger of TON, and robust microglial activation can aggravate
trauma-induced RGCs degeneration, which ultimately leads to RGCs loss.
Toll like receptor 4 (TLR4)-triggered
inflammation is of great importance in
retinal inflammatory response after
optic nerve injury. CD11b on macrophage and brain microglia can inhibit TLR4-triggered
inflammation. However, the functional role of CD11b in
retinal microglia is not well understood. Here, using an optic nerve crush model and CD11b gene deficient mice, we found that CD11b
protein expression was mainly on
retinal microglia, significantly increased after
optic nerve injury, and still maintained at a high level till at least 28 days post crush. Compared with wild type mice, following acute
optic nerve injury, CD11b deficient retinae exhibited more exacerbated microglial activation, accelerated RGCs degeneration, less growth associated protein-43 expression, as well as more proinflammatory
cytokines such as
interleukin-6 and
tumor necrosis factor α while less anti-inflammatory factors such as arginase-1 and
interleukin-10 production. We conclude that CD11b is essential in regulating
retinal microglial activation and neuroinflammatory responses after acute
optic nerve injury, which is critical for subsequent RGCs degeneration and loss.