Effect Of Chronic Immune Response On Brain

During March, many people experience hay fever as a result of excessive immune response. Many people admit that hay fever is not that bad. At the other end of the spectrum there are severe autoimmune diseases like rheumatoid arthritis and multiple sclerosis.

In all these conditions cytokines, molecules that can cause inflammation are seen. A recent research has shed light on the effect of excessive cytokines on neuronal and glial cells in the brain.

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‘In the brain, chronic immune response increases the levels of IL-17A in the hippocampus. This increase in the levels of IL-17A is involved in various neurological diseases like multiple sclerosis, Alzheimer's disease, schizophrenia, and autism spectrum disorder.’
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The research led by Professor Yosuke Takei and Assistant Professor Tetsuya Sasaki at the University of Tsukuba in Japan is published in the journal Neuropsychopharmacology Reports.

The researchers studied an important cytokine called interleukin (IL)-17A and found that chronic increase in the levels of IL-17A circulating in mouse blood can reduce the microglia activity in one part of the brain's hippocampus.

Microglia cells regulate brain development, maintenance of neuronal networks, and injury repair and are related to several neurological diseases.

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The researchers mainly focused on IL-17A as it is known to be involved in neurological autoimmune disorders as well as disorders of the mind. Sasaki explains that it is multiple sclerosis, Alzheimer's disease, schizophrenia, and autism spectrum disorder.

In order to understand how chronically high levels of IL-17A can affect the brain, the team used their knowledge of how IL-17A is made naturally in the body and focused on immune cells called helper T-cells. It was found that with increase in the number of these helper T-cells, called Th17, the mutant mice produced more IL-17A in the gut, which spread throughout the body in the blood.

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IL-17A interacts with two kinds of glial cells in the nervous system, astrocytes and microglia. In one of the region of the hippocampus, a part of the brain that is needed for learning and forming memories, chronically high IL-17A led to reduced activity and density of microglia. On the other hand, astrocytes in the brain did not differ between the mutant and control mice.

This led to believe that chronic IL-17A inflammation would affect cognition, specifically memory but had no effect on spatial memory.

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Takei said, “These mutant mice can be used in future studies as a model for chronic IL-17A-related inflammation. Further neuronal and behavioral testing will help us begin to understand IL-17A's role in a range of debilitating neurological disorders."

Source-Medindia