Why does every desire for sociality fade away when we feel bad? It is an active decision of the brain and immune system, not the symptom of an illness.
“Thanks, but I’m staying home tonight, I don’t feel fit“: how many times have you declined an invitation due to illness? Reducing social contacts to a minimum when you are unwell is not typical of our species alone. Most animals do it to recover energy through rest and avoid the risk of infecting their fellow humans.
According to a new study published in Cellthis mechanism is driven by an active process in which the brain and immune system participate, and is not simply a consequence of the symptoms of the infection. In other words, abstaining from relationships when you feel bad doesn’t just depend on the fact that we don’t feel able to go out: it is instead a self-imposed quarantine a priori by the brain.
Immune messages to the brain
A group of scientists from the Picower Institute for Learning and Memory of MIT used several methods to causally demonstrate that when a component of the immune system reaches specific receptors in a certain brain region, connections are activated that turn off prosociality.
It all starts from interleukin-1 beta, a cytokine, i.e. a protein produced by immune cells during acute infections, which stimulates fever and attracts other immune cells.
This molecular alarm signal reaches its specific receptor (called IL-1R1) on the neurons of a region of the brain called the dorsal raphe nucleus, responsible for modulating social behavior and furthermore located in a point of the brain well supplied by cerebrospinal fluid, which in case of infections is exposed to a “bath” of cytokines.
Proceed by exclusion
Knowing that immune molecules can influence social behavior, scientists tried to inject 21 different types of cytokines into the brains of mice, to understand if any of them could, even in the absence of infection extending to the organism, generate the same effect of withdrawal from sociality generated by a standard infection. Only interleukin-1 beta had this effect.
Then, since this cytokine acts on cells only when it binds to the IL-1R1 receptor, the team looked in which region of the brain these receptors were most widespread, and identified populations of neurons in the dorsal raphe nucleus that expressed it in abundance, many of which were capable of producing serotonin, a neurotransmitter that regulates many basic neural functions. Inhibiting neural activity in this area of the brain or shutting down IL-1R1 receptors prevented withdrawal from social contact in mice, but not the feeling of lethargy caused by the cytokine in question during an infection.
So it is not lethargy directly that makes the desire to meet with others disappear.
Close the circuit
At this point, scientists realized using optogenetics (a technology that allows you to control engineered cells with light pulses) that only activating the connections of the dorsal raphe nucleus with the intermediate lateral septal area caused the observed social isolation behaviors.
In addition to explaining an interesting defense mechanism when we are unwell, the study leaves some questions open. Researchers will have to ascertain whether the neurons with the receptor studied also influence other behaviors during the disease, and whether the serotonin that can be produced by these neurons plays a role in social isolation in the event of infections.
