Psychological stress is a well-known risk factor for illness, but how exactly does it make us sick? A new study has provided some interesting insight.
Researchers at Michigan State University in East Lansing have revealed how a protein known as corticotropin-releasing factor receptor subtype 1 (CRF1) responds to stress by sending signals to specific immune cells.
Study co-author Adam Moeser, of the College of Veterinary Medicine at Michigan State University, and colleagues recently reported their
We all experience stress, and we’ve probably ended up with stress-induced sickness at one point or another. In fact, according to the 2015 Stress in America Survey, around 31 percent of adults in the United States report that stress has a strong or very strong influence on their physical health.
But how is it that psychological stress can make us physically ill? To help shed some light, Moeser and colleagues investigated the effects of stress on mast cells.
Mast cells are immune cells that play a key role in inflammatory and allergic diseases, including asthma, IBS, anaphylaxis, or severe allergic reaction, and lupus.
In response to allergens — such as pollen, dust mites, or peanuts — mast cells release a chemical substance called histamine, which works to rid the body of these allergens. This process is what triggers symptoms of allergy, including watery eyes, runny nose, and airway inflammation.
What are the underlying mechanisms for this stress response, though? This is what Moeser and his colleagues sought to find out.
For their study, the researchers looked at two groups of mice: one that had normal CRF1 receptors on their mast cells, and one that was lacking in CRF1 receptors.
CRF1, also known as corticotropin-releasing hormone, is a peptide involved the body’s response to stress.
In the study, both groups of mice were exposed to psychological stress and allergic stress, wherein the immune system becomes overactive.
The researchers found that the mice with normal CRF1 receptors on their mast cells experienced an increase in histamine levels in response to both stress conditions, and this led to disease.
However, rodents that lacked CRF1 receptors demonstrated low histamine levels in response to stress, and they experienced less disease. Mice that lacked CRF1 receptors saw a 54 percent decrease in disease in response to allergic stress, and a 63 percent decline in disease in response to psychological stress.
According to Moeser, these findings show “that CRF1 is critically involved in some diseases initiated by these stressors.”
“Mast cells,” he explains, “become highly activated in response to stressful situations the body may be experiencing.”
“When this happens,” he goes on to say, “CRF1 tells these cells to release chemical substances that can lead to inflammatory and allergic diseases such as irritable bowel syndrome, asthma, life-threatening food allergies, and autoimmune disorders such as lupus.”
While further studies are required, the team believes that the findings could open the door to new treatments for stress-induced illness.
“We all know that stress affects the mind-body connection and increases the risk for many diseases,” says Moeser. “The question is, how?”
“This work is a critical step forward in decoding how stress makes us sick and provides a new target pathway in the mast cell for therapies to improve the quality of life of people suffering from common stress-related diseases.”