Researchers have identified clusters of immune cells in the gut of Crohn's disease patients that may be driving the development of excess scar tissue (fibrosis). This breakthrough could lead to new treatments aimed at preventing or slowing this serious complication.
Crohn’s disease causes inflammation of one or more parts of the intestines, which can eventually lead to fibrosis of the affected tissue. — Prof IDA NORMIHA HILMI Scientists believe they have identified what drives the development of scar tissue in the intestines of people with Crohn’s disease.
The University of Edinburgh-led researchers in Britain found clusters of immune cells in the gut that may be stimulating nearby cells to generate excess scar tissue – a process known as fibrosis., could help develop treatments to prevent or slow the development of fibrosis, a serious complication of Crohn’s disease.Over time, the ongoing inflammation can lead to fibrosis, where excess collagen builds up in the bowel wall.The research team hope that the latest findings could help pinpoint therapeutic targets that could be explored to interrupt the scarring process and develop treatments specifically aimed at fibrosis. University of Edinburgh honorary senior clinical lecturer and NHS Lothian consultant gastroenterologist Dr Shahida Din said: “Fibrosis remains one of the most challenging complications of Crohn’s disease because current treatments primarily target inflammation rather than the scarring itself. “Understanding the cellular signalling pathways that link immune activity to collagen production could help guide the development of therapies aimed at preventing or slowing fibrosis.” The research team analysed intestinal tissue samples from Crohn’s disease patients with fibrosis, focusing on the ileum – the final part of the small intestine where the disease most commonly develops. They used archived intestinal tissue samples to examine structural changes across the different layers of the bowel wall. They found significantly increased fibrosis and immune cell infiltration in Crohn’s disease tissue, compared with normal tissue. The submucosa – a deeper layer of the bowel wall – had particularly high levels of scarring, indicating that it may play an important role in the early stages of fibrosis. The researchers next analysed fresh intestinal tissue samples using a cutting-edge technique to study gene activity in individual cells, known as single-cell RNA sequencing. They identified a link between clusters of immune cells, known as Crohn’s lymphoid aggregates, and groups of endothelial cells, which normally line blood vessels. The scientists found that the endothelial cells appeared to form distinctive structures surrounding the Crohn’s lymphoid aggregates. Further analysis revealed signalling interactions between these clusters and nearby cells responsible for producing collagen, suggesting that they may actively promote fibrosis. University of Edinburgh postdoctoral research fellow Dr Michael Glinka said: “Our findings highlight previously unrecognised interactions between immune cells, endothelial cells and collagen-producing cells in Crohn’s disease. “By combining traditional pathology with single-cell transcriptomics, we were able to confirm these changes using two independent approaches and uncover biological signalling pathways that may provide new therapeutic targets.” Service, Research and Evidence director Catherine Winsor of the British charity Crohn’s & Colitis UK, said: “People who live with Crohn’s often tell us how much fibrosis and scarring can affect their lives, yet it’s something current treatments don’t address. “This early research is really exciting because it helps us to understand what drives that scarring and where new treatments could make a difference. “It brings real hope that, in the future, we might be able to treat not just inflammation, but the lasting damage Crohn’s can cause.” – PA Media/dpa
Crohn's Disease Fibrosis Scar Tissue Immune Cells Intestinal Inflammation
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