Gaps In Intestinal Barrier Could Cause Crohn’s Disease

Scientists at the University of Liverpool believe gaps in the intestinal barrier could be a cause of inflammatory diseases of the gut such as Crohn’s Disease.

Their research, led by Professor Alastair Watson in the University’s Faculty of Medicine, could have important implications for the treatment of patients with diseases like Crohn’s – an inflammatory bowel disorder that causes severe ulceration in the intestine, leading to pain, bleeding and diarrhoea.

Professor Watson’s research has concentrated on the renewal of epithelial cells in the lining of the bowel and the ‘gaps’ in the lining that the process leaves behind.

The human bowel is lined with millions of projections called villi which increase the surface area of the intestine to allow for the efficient absorption of nutrients. The villi are covered in epithelial cells which are constantly renewed – around a thousand billion cells are shed from the top of the villi every day.

Professor Watson and his team found that this renewal process leaves ‘gaps’ in the lining of the bowel which, in healthy tissue, are immediately filled with a glue-like substance that plugs the gaps. The research team, discovering these gaps for the first time, found that around 3% of the bowel’s surface area is covered in this substance. It was previously assumed that the lining of the intestine was a continuous sheet of cells.

Professor Watson said: “We suspect that patients with inflammatory disease may not have the same ability to plug the gaps left by the cell renewal process – meaning that bacteria can seep through the lining of the intestine. Understanding this cell shedding process may lead to new treatments for inflammatory bowel disease.”

He added: “Our research may also explain the development of colon cancer which we believe may be down to a failure in the renewal process of epithelial cells. If they don’t renew but amass on the wall of the gut, they may develop into a cancer – it’s an area we’ll be concentrating on in the next stage of our study.”

The research, published in Gastroenterology, was carried out in collaboration with the University of Cincinnati.