JUN 14, 2018 06:36 PM PDT

Learning how Irritable Bowel Syndrome Starts

WRITTEN BY: Carmen Leitch

Over ten percent of the world’s population is affected by irritable bowel syndrome and disease, and now scientists have learned more about an early cause of the disorder. The work, by researchers at Michigan State University, has been reported in Cellular and Molecular Gastroenterology and Hepatology. The investigators have found that the communication between a type of cell called enteric glia and neurons in the gut is to blame.

Michigan State University scientists have identified an early cause of intestinal inflammation, one of the first stages of inflammatory bowel disease and irritable bowel syndrome, which afflict around 11 percent of the world's population. / Credit: Courtesy of MSU

"The gut has its own brain, and that has more neurons in the intestines than in the spinal cord. Within your intestines lies a 'second brain' called the enteric nervous system," explained the senior author of the report, Brian Gulbransen, MSU neuroscientist. "The enteric nervous system is an exceedingly complex network of neural circuits that programs a diverse array of gut patterns and is responsible for controlling most gastrointestinal functions."

Along with the neurons in the gut that form the so-called second brain, enteric glia act to control inflammation. That inflammation can disrupt the connections between neurons in the gut, which is known to play a major role in the development of inflammatory bowel disease. 

Neurons in the gastrointestinal tract make a molecule called tachykinins, which are peptides that can induce inflammation in the gut. Tachykinins are important to intestinal muscle contractions, and the transmission of pain signals. The researchers found that even before rumblings and pain starts, molecular changes are happening. Tachykinins can encourage inflammation in enteric neurons, enteric glia and structures called TRPV1-positive nerve fibers.

Glial cells had been thought to just have functions in supporting roles, but the researchers found that they are apparently actively involved in signaling in the gastrointestinal system. 

"Post inflammation, there are still many angry glial cells. Because they've amped up their signaling, they make you, and your gut, more sensitive," Gulbransen said. "We hope we can turn them back to happy glia, reduce the sensitivity and return gut function to normal."

An important player in this system is a receptor called NK2R, which is vital to the communication between neurons and glia. The researchers are continuing their work to try to learn about the genes that are involved. They are intrigued by one in particular, NK2R.

"By blocking the receptor with GR 159897, which is a known NK2 receptor antagonist drug, it disconnected the signaling between neurons and glia," he said. "It proved to be quite effective in accelerating recovery from inflammation."

This work may help create therapeutics for reducing inflammation or resetting the sensitivity of gut neurons.


Sources: AAAS/Eurekalert! via Michigan State University, Cellular and Molecular Gastroenterology and Hepatology

About the Author
  • Experienced research scientist and technical expert with authorships on 28 peer-reviewed publications, traveler to over 60 countries, published photographer and internationally-exhibited painter, volunteer trained in disaster-response, CPR and DV counseling.
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