Why is it worse with a cold?

The depressed psychoemotional state during an illness can occur due to the chemical signals that the immune system sends to the brain.

The most unpleasant thing in any cold is probably not a cough or a runny nose, but what is called a “fog in the head”: a constant feeling of apathy, fatigue, inability to concentrate on anything, etc. The reasoning is that the disease takes away strength, does not explain anything, because it is not clear how she takes away strength for mental work, how she deprives of emotions, how she manages to lead us into a depressed mental state?

Obviously, the disease somehow affects our brain. But if we are talking about the same cold, then the rhinoviruses that cause it, multiply in the mucous membrane of the nasopharynx, they do not need a brain at all. Maybe the whole thing in the immune response to the disease? Although there is a so-called blood-brain barrier between the brain and the circulatory system that neither pathogens nor immune cells and molecules pass into the brain, exceptions sometimes do happen: several examples are now known that the signals of the immune system can still pass through the barrier.

Thomas Blank and his colleagues at the University of Freiburg, the Ruhr University and the University of Heidelberg conducted several experiments with mice infected with a short-term viral infection. Since researchers were interested in the behavior and in general the psychological state of the animals, they were subjected to the following test: sick mice were put in a trough with water, from which it was very difficult to get out without help, and watched what they would do.

Healthy animals tirelessly tried to get to the land, despite the futility of attempts, but the patients quickly refused to fight and just tried not to drown, swimming in the “pool”. That is, sick animals became more apathetic, more indifferent, more depressive.

According to the authors of the work in their article in the journal Immunity, in response to infection, mouse immunity increased the level of beta-interferon. In general, interferons are one of the main antiviral agents: first, they force immune molecules to attack viral proteins, secondly, interferons act on infected or threatened cells, suppressing protein synthesis in them, launching a self-destruct program, etc.

It turned out that the beta interferon in question is able to bind to the receptors of the cells that make up the blood-brain barrier in the blood vessels of the brain. When this receptor was turned off in mice, the animals became more resistant to the inhibitory effects of the disease.

Being infected (RNA molecules were used as an infection, which act on immunity in the same way as a virus), mice showed greater persistence in seeking to get out of the water onto dry land; and at the same time, they had better memory — when a platform was being made into the water maze, mice without a receptor could better remember where it was located.

At the molecular-cellular level in the brain of animals, the following occurred: because of the virus, immunity, as was said, increased the level of beta-interferon, which acted on the receptors of blood vessels and thereby stimulated the synthesis of a small immune protein CXCL10.

This cytokine protein weakened the memorizing ability of the hippocampal neurons (as we know, the hippocampus is one of the main memory centers). On the one hand, we can see how the immune signal passes through the notorious blood-brain barrier – using interferon receptors on barrier cells and the CXCL10 protein, which already works on the other side of the barrier. On the other hand, immunity really affects the activity of neurons; Although the authors of the work speak only of hippocampal cells and learning ability, it is possible that the same or similar immune signal can reach the neural chains that control emotions.

True, some researchers speak about the results with a certain degree of skepticism. For example, Robert Danzer (Robert Dantzer) from the Cancer Center. MD Anderson at the University of Texas says that the cytokine immune signal beaks, which include CXCL10, act locally, in the focus of infection, and therefore there are certain doubts that the same CXCL10 can go somewhere far into the bowels of the brain. Although it may well be that there are still some signaling molecules involved that react to CXCL10 and spread its influence to “remote areas”.

There is still need to keep in mind that there are other types of immune response when the antiviral properties of interferon are not needed; and, for example, in inflammation caused by bacteria, some other mechanisms may be triggered, which also lead to general lethargy.

From an evolutionary point of view, everything is correct here: psychological inhibition does not allow the patient to expend the energy that may be needed to fight the infection. But in general, it would be nice if we could interrupt the immune signals, forcing us to dive into such an “infectious depression” – now we live easier than hundreds of thousands of years ago, and perhaps the immunity does not have to worry so much about saving energy to fight the virus.

Finally, exactly the same signs of an oppressed psycho-emotional state occur in cancer patients and patients with autoimmune disorders treated with immunotherapy — and for them some remedy to get rid of the immune “fog in the head” would also be very helpful.

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