LIFE SCIENCE

Chronic stress thus inflames the intestines


Psychological stress is known to aggravate digestive tract inflammation caused by certain intestinal disorders. Now, American scientists have figured out why. The paper was published May 25 in Cell.

The new study presents a comprehensive narrative — a process that starts with chemical signals produced by the brain and ends with immune cells in the gut — a process that causes trouble for people with these diseases.

Intestinal tissue (artificial staining) in patients with ulcerative colitis. Photo by Steve Gschmeissner/Science Photo Library

This study helps explain how chronic stress triggers physical distress. This means that the level of stress managed can have a profound impact on the outcome of treatment for inflammatory bowel disease (IBD).

Author Christoph Thaiss, a microbiologist at the University of Pennsylvania in Philadelphia, said the idea runs counter to traditional medical approaches, which “completely ignore the patient’s psychological state as the main driver of treatment response.”

Abdominal pain, diarrhea, and fatigue are just some of the symptoms experienced by people with IBD. The two main IBDs, ulcerative colitis and Crohn’s disease, are mild for some but can be debilitating or even life-threatening for others.

Stressful events, such as losing a job or breaking up with a partner, are often precursors to the onset of IBD. Thaiss and colleagues have found that connection. After a surge in stress, the brain signals to the adrenal glands, which release chemicals called glucocorticoids to other parts of the body.

Initially, the researchers considered the idea that glucocorticoids act directly on immune cells, which respond by releasing molecules that cause inflammation.

“But it turns out there’s a layer in between.” Thaiss said. They found in mice that glucocorticoids act on intestinal neurons and glial cells that connect intestinal neurons.

After being activated by glucocorticoids, some glial cells release molecules that trigger immune cells. In turn, these immune cells release molecules that are normally used to fight pathogens, but in this case, end up causing painful intestinal inflammation.

At the same time, the researchers found that glucocorticoids prevent immature intestinal neurons from fully developing. As a result, these neurons produce only low levels of signaling molecules that cause the intestinal muscles to contract. This means that food moves slowly through the digestive system, which increases the discomfort of IBD.

The researchers were surprised to find that glucocorticoids cause inflammation in the gut, as these compounds are sometimes used to treat IBD. This apparent contradiction can be explained by the short-term pattern of using this method of treatment.

Thaiss explained that while the rapid burst of glucocorticoids appears to have anti-inflammatory effects, when stress becomes chronic, “the system changes completely” and glucocorticoids begin to exert pro-inflammatory effects.

John Chang, a gastroenterologist and immunologist at the University of California, San Diego, said it was a “reasonable explanation.”

Thaiss said the brain’s ability to drive inflammation “seems to be much more powerful than previously thought.” This suggests that IBD treatment medications, combined with stress management approaches, may be more effective than drugs alone.

At the same time, molecules in signaling pathways from the brain to the gut are expected to be targets for new drugs. “An exciting possibility.” Chang said.

In addition, stress is also thought to exacerbate inflammatory diseases of the skin and lungs, possibly through similar signaling pathways. So the implications of this study may extend beyond IBD.

“We need to continue to explore the brain, and how it controls seemingly unrelated physiology and disease.” Thaiss said. (Source: Wang Fang, China Science News)

Related paper information:https://doi.org/10.1016/j.cell.2023.05.001



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