The Immune System Can Trigger Anxiety In Response To An Infection

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In recent years, scientists have discovered interesting links between immunity and the brain. In fact, one of the immune signaling molecules, or cytosines, involved in these compounds is called interleukin-17a (IL-17a).

This molecule plays an important role in psoriasis, an autoimmune skin disease, but it can also contribute to the depression that many people experience. In this regard, a study using a mouse model of psoriasis found that IL-17a caused symptoms similar to those of depression.

In humans, researchers have linked the molecule to treatment-resistant depression. Research in mice has even implicated IL-17a in the development of autism.

 “The brain and the body are not as separate as people think,” says Professor Jonathan Kipnis, a neuroscientist at Washington University School of Medicine in St. Louis. While working in medical school, the professor and his colleagues discovered that IL-17a causes anxious behavior in mice. 

Therefore, they are investigating whether too much or too little of this molecule could be linked to anxiety in humans.

T GAMMA-DELTA CELLS

Immune cells called gamma delta T cells produce IL-17a. These cells are found in the meninges, the membranes that surround the brain and the spinal cord.

To determine what effect IL-17a might have on behavior, the scientists studied mice whose gamma-delta T cells did not produce IL-17a and mice which did not at all.

In this way, they subjected the mice to standard tests of memory, social behavior, foraging, and fear. The mice performed as well as the normal mice in all tests except for two which measured anxiety levels.

In these tests, mice that did not have gamma delta T cells or that did not produce IL-17a were more likely to explore open areas. In the wild, this type of behavior would put them at a greater risk of being eaten by predators. The researchers interpreted this as a sign of reduced anxiety in animals without IL-17a signaling in their central nervous system.

Scientists then studied how it affects the signal from neurons to the brain, and they found receptors for IL-17a on a type of stimulating nerve cell called a glutamatergic neuron.

When neurons were genetically modified to prevent them from producing these receptors, mice exhibited less anxious behavior.

The gut-brain axis

Previous animal research has revealed many possible links between bacteria living in the gut and behavior, including fearful behavior. This connection is known as the gut-brain axis, and scientists have suggested the immune system as a possible way to exchange messages with each other.

To study the role of IL-17a in the gut-brain axis, Alves de Lima and his colleagues injected mice with lipopolysaccharide. It is a toxin produced by bacteria that causes a strong immune response.

In response to this injection, gamma delta T cells in the meninges surrounding the brains of animals produced this type of molecule. In another experiment, when researchers treated mice with antibiotics to kill bacteria in their gut, the animals produced less IL-17a.

Taken together, the results of these experiments suggest that the immune system evolved not only to fight infections, but also to modify behaviors to protect animals while being weakened.

The team is currently studying how gamma delta T cells in the meninges surrounding the brain can detect the presence of bacteria in other parts of the body.

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