An iron-regulating molecule called hepcidin is produced by the immune system and restricts the growth of gut bacteria after an intestinal injury, helping to heal the lining of the intestine, according to a study by Weill Cornell Medicine, NewYork-Presbyterian and Institut Cochin investigators.
The study, published April 10 in Science, was conducted in mice and human samples and could have important implications for treating gastrointestinal diseases that damage the lining of the intestines as a result of infection, chronic inflammation or cancer. Currently, most treatments for gut-damaging conditions like inflammatory bowel disease (IBD) focus solely on reducing inflammation and do not directly address the need to promote tissue repair.
“Not being able to heal your intestine is a major problem in patients with inflammatory bowel disease and other gastrointestinal disorders,” said senior author Dr. Gregory F. Sonnenberg, associate professor of microbiology and immunology in medicine in the Division of Gastroenterology and Hepatology and a member of the Jill Roberts Institute for Research in Inflammatory Bowel Disease at Weill Cornell Medicine. “There is an urgent need to better understand the pathways that promote mucosal healing and harness that knowledge to design new treatment strategies.”
Bleeding in the intestines is often one the first signs of diseases like IBD or colorectal cancer, said lead author Dr. Nicholas Bessman, a postdoctoral associate in medicine at Weill Cornell Medicine. Intestinal bleeding may further exacerbate these diseases or hamper healing by fueling overgrowth of gut bacteria. This happens because blood contains large amounts of iron, which is essential for bacterial growth. To investigate the potential role of the iron-regulator hepcidin, the team collaborated with Dr. Carole Peyssonnaux and other researchers at the Université de Paris, INSERM, Institut Cochin, and examined intestinal healing in mice with and without the hepcidin gene. To read further, please click here.
From left: Drs. Robbyn Sockolow and Gregory Sonnenberg
Dr. Nicholas J. Bessman