For the first time, cells involved with the communication between stress responses in the brain and inflammation in the gastrointestinal (GI) tract have been identified, according to findings from the Perelman School of Medicine. In a study published in Cell, researchers have discovered in animal models that glial cells, which support neurons, communicate stress signals from the central nervous system (CNS) to the semi-autonomous nervous system within the gastrointestinal (GI) tract, called the enteric nervous system (ENS). These psychological stress signals can cause inflammation and exacerbate symptoms of inflammatory bowel disease (IBD).
An estimated 1.6 million Americans currently have IBD, which refers to two conditions—Crohn’s disease and ulcerative colitis—characterized by inflammation of the GI tract, and can cause symptoms like persistent diarrhea, abdominal pain, and bloody stools. Prolonged inflammation can also lead to permanent damage to the GI tract. Current treatments consist of anti-inflammatory drugs, immune suppressants, dietary changes, and steroids.
“Clinicians have long observed that chronic stress can worsen IBD symptoms, but until now, no biological connection has been identified to explain how the digestive system knows when someone is stressed,” says senior author Christoph Thaiss, an assistant professor of microbiology.
In the study, researchers traced initial stress response signals to the adrenal cortex, which releases glucocorticoids—steroid hormones that activate the physiological responses to stress throughout the body. The researchers found that neurons and glia in the ENS responded to chronically elevated glucocorticoid levels, suggesting that they are the link between stress perception by the brain and intestinal inflammation.
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