The intestinal lining is an important tissue. Among its other functions, it protects the body from inflammation that can be generated by the actions of gut microbes. This barrier declines with age, and this is thought to be influential in the increased chronic inflammation observed in older people. Ways to spur greater maintenance and repair on the part of cell populations making up intestinal tissue would likely be of great benefit, given the importance of chronic inflammation as a driver of age-related disease.
A strong cellular lining is essential for a healthy gut as it provides a barrier to the billions of microbes and harmful toxins present in our intestinal tract. This barrier is often damaged by infection and inflammation, which causes many painful symptoms. Researchers investigated the environment that surrounds gut stem cells and used “mini gut” organoid methodology where tiny replicas of gut tissue were grown in a dish. The study defined key cells that reside in close proximity to stem cells in the gut that produce the biomolecule Neuregulin-1 (NRG1) that acts directly on stem cells to kick-start the repair process.
“Our really important discovery is that supplementation with additional Neuregulin-1 accelerates repair of the gut lining by activation of key growth pathways. Our findings open new avenues for the development of Neuregulin 1-based therapies for enhancing intestinal repair and supporting rapid restoration of the critical gut function.”
Gastrointestinal disease, such as Crohn’s disease and ulcerative colitis, is a major health issue worldwide and results in severe damage to the epithelial cell layer lining the gut. Under these conditions, the intestine has a limited capacity to repair efficiently to restore its main absorptive function and is associated with symptoms including diarrhoea, dehydration, loss of weight and malnutrition. Developing ways to support intestinal tissue repair will dramatically improve patient recovery.
Link: https://www.eurekalert.org/pub_releases/2020-07/mu-htr072020.php