Intestine neurons produce a molecule that plays a central role in the formation of the immune response of the intestine during and after inflammation, according to a new study by Weill Cornell Medicine Investigators. The results suggest that targeting these neurons and the molecules they produce could open the door to new treatments for the inflammatory intestine disease and other disorders driven by intestinal inflammation.
Hundreds of millions of neurons constitute the enteric nervous system, the “second brain” of the body, where they orchestrate the essential functions of the intestine such as the displacement of foods through the intestines, the absorption of nutrients and blood flow. Although this system is known to regulate these fundamental processes, its role in controlling intestinal inflammatory responses has remained much less clear.
In their study, reported on August 15 in nature immunology, researchers focused on group 2 innate lymphoid cells (ILC2S), immune cells that reside in intestine coatings. Their previous work has revealed that ILC2 is a major source of a factor of growth in tissue healing called amphiregulin and have the capacity to receive neural signals which modulate their function and can have an impact on the progression and recovery of the disease. In the new study, they demonstrated that the tissue protection function of ILC2 depends on the production of a molecule called adrenomedullin 2 (ADM2) of the enteric nervous system; The administration of the molecule has expanded this group of ILC2 and provided therapeutic advantages in a preclinical model of inflammatory intestine disease, while the loss of the ADM2 signaling exacerbated a disease due to the absence of these protective cells.
The enteric nervous system has long been neglected when we can resolve the prejudicial intestinal inflammation. Our work suggests that there can be a neuro-immune mechanism previously unknown leading to responses from intestinal healing. “”
post-doctoral Fellow Nih Ruth L.
In addition, investigators carried out translational studies based on patients by analyzing human tissues and blood samples from the Weill Cornell Medicine’s inflammatory intestine Institute. This analysis revealed that patients with an inflammatory intestine disease had a high expression of ADM2 compared to witness individuals and found that humans were stimulated with Adm2 directly favored the production of protective tissue amphirian. These results indicate that communication of the immune system identified in mice is also present in humans, highlighting the enteric nervous system as a promising therapeutic target for the inflammatory intestine disease.
“The results of this current study allow new knowledge of how immune and nervous systems are talking about and coordinate complex processes, including inflammation and fabrics, and offer the potential of new therapies targeting these neuro-immune interactions,” said Dr. David Artis, director of Jill Roberts, author of intestine medicine and Michael Kors, The medicine of the switch Michael Allen Discovery Center for neuro-immune interaction.
