U.K. scientists have made a significant discovery about what causes inflammatory bowel disease (IBD), which could lead to new treatments. A joint study between the Francis Crick Institute and University College London found a common genetic factor in 95 percent of IBD patients that makes their immune cells more likely to cause inflammation in the gut.
IBD is an umbrella term for two conditions – Crohn’s disease and ulcerative colitis – characterized by chronic inflammation of the gastrointestinal tract. Common symptoms include diarrhea, abdominal pain and cramps, rectal bleeding, weight loss, and fatigue.
Using genetic analysis, the researchers discovered a region of DNA that is the “master regulator” of macrophages – a type of white blood cell that drives inflammation in people with IBD. It boosts the activity of a gene called ETS2, which controls the inflammatory chemicals the macrophages release, with higher levels of ETS2 correlating with more inflammation. Some people have a version of the genetic code that makes their body prone to responding excessively to an inflammatory stimulus.
While specific drugs to block ETS2 don’t exist, the researchers discovered that medications prescribed for other conditions could calm excessive inflammation. Specifically, MEK inhibitors, used to treat cancer, showed great potential. However, these drugs can have serious side effects, so scientists are now working on adjusting the drugs to target just the macrophages.
The plan is to start clinical trials in the next five years to test if the newly calibrated drugs are safe and effective for IBD patients. This research, published in the journal Nature, helps answer critical questions about IBD and brings us closer to finding better ways to manage and potentially cure these lifelong conditions.