Researchers have identified a key mechanism that slows tissue repair in patients with inflammatory bowel disease. An advance that could open the way to new treatments.
- A new study reveals a specific mechanism that inhibits intestinal repair in patients with inflammatory bowel diseases (IBD), such as Crohn’s disease.
- A protein, interferon lambda (IFN-λ), blocks mucosal regeneration by activating a molecular cascade that destroys intestinal stem cells. This process, designed to eliminate infected cells, remains active even after the acute phase of inflammation.
- Blocking IFN-λ could promote wound healing and improve remission. This opens new perspectives for IBD treatments.
Inflammatory bowel diseases (IBD), which affect more than 250,000 people in France, include Crohn’s disease and acute ulcerative colitis. They manifest as chronic inflammation of the intestine causing abdominal pain and diarrhea. While current treatments, such as anti-inflammatories, alleviate symptoms, only half of patients achieve complete remission. For others, the intestinal mucosa remains partially healed, increasing the risk of relapses.
An international study, published in the journal cellhowever, has just shed light on a key mechanism that prevents complete healing of the intestines in affected patients. A discovery that could revolutionize treatments against these particularly debilitating chronic pathologies.
A molecular pathway that prevents gut repair
Scientists from several research centers, including the CNRS, have highlighted the unexpected role of interferon lambda (IFN-λ) – a protein normally involved in the fight against viruses – in slowing down repair of the mucosa. intestinal. In patients with IBD, this protein blocks the regeneration of the epithelial layer of the intestine, essential for its repair.
Using transgenic mouse models and intestinal organoids (“mini-intestines” grown in the laboratory), scientists were able to trace the molecular pathway activated by IFN-λ. They found that the abnormally high protein stimulates excessive production of ZBP1, another molecule that triggers the destruction of intestinal stem cells.
However, this mechanism, designed to eliminate cells infected by viruses, is disrupted in IBD. Even in the absence of infection, chronic inflammation can activate ZBP1, preventing intestinal repair. Even more surprising, this mechanism remains active beyond the acute phase of inflammation, slowing healing even when current treatments reduce inflammation. “This finding is particularly important in a therapeutic context, as current therapies can calm inflammation but often do not result in complete cure.”specifies the CNRS in a press release.
Towards a new therapeutic approach
These discoveries open up promising perspectives, say the researchers. By blocking lambda interferons, it would be possible to restore the regenerative capacity of the intestines. This would not only improve healing, but also the quality of life of patients, while reducing the risk of serious complications.
For scientists, this study also illustrates the importance of rethinking therapeutic strategies. Rather than just calming inflammation, future therapies could target repair of damaged tissue, giving patients a chance for true and lasting remission.
