Microglia protect the central nervous system from inflammation and could hold the key to treating retina disease

Microglia help protect the central nervous system from disease-causing pathogens and issues. Recent research has revealed that these cells determine whether or not other immune cells might enter the brain. Managing these gatekeeper cells might offer a way to control the risk of inflammation that damage the retina.

Researchers at the Massachusetts Eye and Ear (MEE) hospital discovered the role of microglia while studying a model of autoimmune uveitis. The disease accounts for around 10 percent of the global cases of blindness around the world.

Microglia play a role in kicking off autoimmune uveitis in the central nervous system. They orchestrate inflammation in the retina, which damages the eye and impairs the sight.

When the disease appeared in the brain, the immune cells linked themselves with the blood vessels in the retina. Microglia controlled the entry of inflammation-causing immune cells through the blood-brain barrier.

The researchers eliminated microglia in their experiment. They found that doing so prevented autoimmune uveitis from developing in the retina.

Their findings were published in the journal Proceedings of the National Academy of Sciences (PNAS). (Related: Can an unbalanced diet negatively affect your eye health?)

Microglial cells are the gatekeepers to the brain

“Normally, the blood brain barrier serves as an impediment and prevents the immune response from going into tissues of the central nervous system, including the retina,” explained MEE researcher Dr. Kip M. Connor. “However, our results provide clear evidence, that in the context of uveitis, microglia can facilitate entry of inflammatory immune cells into the retina, and enable the host immune responses to attack cells that are not normally recognized by the immune system.”

Connor elaborated that the gatekeeper role of microglia made them a potential means of preventing uveitis from taking place in the retina. In addition to keeping inflammation-causing immune cells out of the eye, microglia might also get stimulated to permit the passage of other chemicals through the blood-brain barrier.

Autoimmune diseases like Bechet’s disease, sarcoidosis, and Vogt-Koyanagi-Harada disease may trigger uveitis. Patients suffer from severe inflammation in their optic nerve, retina, uveal tissues, and vitreous.

Persistent inflammation due to excessive immune response inflicts damage upon the neuronal cells of the retina. As a result of the inflammatory damage, patients often experience considerable loss of vision.

It so happens that plenty of immune cells enter the eye around the same time that inflammation rages unchecked in the central nervous system.

Microglia may help or harm the body during certain diseases

Microglia possess many phenotypes and various stages of activation. They may exert either beneficial or harmful effects during the development and progression of a disease.

In recent years, researchers have started figuring out the roles of microglial cells in many diseases. They are believed to contribute to the onset of neurodegenerative diseases like Alzheimer’s disease and Parkinson’s disease.

In ophthalmology, microglial cells respond to developments and indications of disease. Depending on the context of the condition, they may either protect against illness or contribute to its progression.

MEE researcher Dr. Yoko Okunuki said that their findings shed light on how microglia react and work during a systemic autoimmune disease that affects the eye.

“This novel work by Dr. Connor and colleagues identifies that microglia regulate entry through the blood-retinal barrier, and it is our hope that these finding can be harnessed for future targeted therapies for uveitis,” commented MEE researcher Dr. Joan W. Miller, who didn’t participate in the study.

“It is becoming increasingly clear that microglia are involved in a number of retinal disorders as well as neuroinflammatory disorders of the central nervous system.”

Sources include:

Newswise.com

PNAS.org