Inflammation of the respiratory tract could result from exposure to smoking or air pollution
LYSENKO Andrii / Shutterstock
Severe inflammation of the respiratory tract alters the ability of mice to learn when a dangerous situation is no longer a threat, which suggests that the lungs influence emotions and behavior. This pulmonary brain connection could also help explain why only a fraction of people who undergo trauma develop a post-traumatic stress disorder (SSPT).
“Many of us see trauma, but only about 5 to 10% of people exposed to trauma really get the SSPT,” said Renu Sah at the University of Cincinnati in Ohio. Previous research indicates that inflammation, especially in the lungs, could play a role. For example, among military veterans, people with SSPTs are about eight times more likely to have asthma.
Sah and his colleagues have also studied this link in eight mice with serious symptoms of the type of asthma. They exposed the lungs of animals to dust mites, which sparked an allergic reaction and inflammation. Three days later, they placed the mice in a cage and gave them three light electric shocks.
During the next six days, the researchers returned the mice in the cage for 5 minutes a day, recording how long they stood frozen for fear. On average, they spent around 40% of their last frozen session – twice as long as a separate group of 11 mice which had no pulmonary inflammation and which were also exposed to electric shocks.
There was no difference in the frost between the two groups the day after the shocks, indicating that the two developed a fear response. However, the fact that the first mouse group was so much frightening a few days later suggests that a serious inflammation of the respiratory tract interferes with the capacity of the brain to recognize when a previous threat has passed. “In patients with SSPT, this process does not work well, which is why they have a memory of prolonged fear,” says Sah.
The researchers repeated this experience in a group separated from mice suffering from severe pulmonary inflammation, but this time administered a medication that blocks the activity of an inflammatory molecule called interleukin-7A. During their last session in the cage where they had previously received shocks, these animals spent about half of the time frozen for fear that those who did not get the medication.
Other tests have revealed that immune cells in a brain region known as the subordinate organ have receptors for this molecule. Unlike most of the brain, the subngical organ does not have a blood-brain barrier, the closely sealed cell of cells that prevent most of the blood from reaching neurons. As such, he acts as a “window on the brain”, which allows him to keep an eye on what is happening in the body and react accordingly, explains Sah.
She and her colleagues have found that immune cells in this region detect inflammatory lung molecules, which activates nearby neurons. They then point out the infralimbic cortex, a brain area involved in the recognition of the moment when a threat has passed.
Researchers inhibited this path in mice with severe pulmonary inflammation using specialized drugs, a technique called chemiogenetics, which has considerably reduced the time they frozen in fear after being shocked.
“Thus, in a word, pulmonary inflammation, in particular severe pulmonary inflammation, can have an impact on a higher cortical function and your ability to treat traumatic experiences,” explains SAH. A similar route probably exists in people, because the brain circuits that governs fear are similar between the two species, she says.
Other studies have shown that chronic psychological stress reduces immune responses. Sah suspects that the opposite occurs here: that an increased immune response decreases psychological functions, as well as recognition from the moment when a threat has passed. This may be due to the fact that the body redirects its resources away from the brain to cope with the threat in the lungs, she said.
“This research is important to better understand how body and mind are connected,” explains Douglas Vanderbilt at the Los Angeles children’s hospital. This could also explain why his own research has shown that children with serious asthma have more serious SSPT symptoms. “But I think what we learn is that these brain interactions are very complicated, so it’s probably not the only way.” For example, the psychological stress of asthma attacks could also influence the risk of the SSPT, he says.
The study only used male mice, so that the tracks can also differ in women, explains SAH, and can therefore also vary between men and women, which requires a more in -depth study.
However, these results could help us better identify people who are more vulnerable to the SSPT. For example, doctors may want to filter children with serious asthma for the mental health problem, explains Vanderbilt. This could also lead to new SSPT treatments, such as immune therapies that mitigate inflammation, he says.
Subjects:
