Scientists have made a significant breakthrough in understanding Crohn's disease, identifying what drives the development of debilitating scar tissue in the intestines. University of Edinburgh-led research suggests clusters of immune cells within the gut stimulate surrounding cells to produce excessive scar tissue, known as fibrosis.
This crucial insight offers hope for developing treatments to prevent or slow fibrosis, a severe complication of the chronic inflammatory condition. Crohn's disease affects the digestive tract and involves persistent inflammation leading to fibrosis, in which excess collagen builds up in the bowel wall. This scarring can narrow and block the intestine, and often requires surgery.
Researchers analysed intestinal tissue samples from Crohn's disease patients with fibrosis, focusing on the ileum. They found significantly increased fibrosis and immune cell infiltration in Crohn's disease tissue compared with normal tissue. Using single-cell RNA sequencing, they identified a link between clusters of immune cells, known as Crohn's lymphoid aggregates, and groups of endothelial cells. Further analysis revealed signalling interactions between these clusters and nearby cells responsible for producing collagen.
Dr Shahida Din, consultant gastroenterologist at NHS Lothian and honorary senior clinical lecturer at the University of Edinburgh, said: 'Fibrosis remains one of the most challenging complications of Crohn's disease because current treatments primarily target inflammation rather than the scarring itself.' Dr Michael Glinka, research fellow at the University of Edinburgh, added: 'Our findings highlight previously unrecognised interactions between immune cells, endothelial cells and collagen-producing cells in Crohn's disease.'
The study was conducted by a UK-wide collaboration and funded by the Leona M and Harry B Helmsley Charitable Trust. Catherine Winsor, director of service, research and evidence at Crohn's & Colitis UK, said: 'This early research is really exciting because it helps us to understand what drives that scarring and where new treatments could make a difference.'
