June 6, 2024 – Scientists within the United Kingdom have identified genetic aspects that appear to cause the event of inflammatory bowel disease, and laboratory experiments with existing drugs used for other conditions show that these drugs could possibly be an efficient treatment.
Inflammatory bowel disease (IBD) is the collective term for Crohn's disease and ulcerative colitis, each of which cause chronic inflammation within the gastrointestinal tract. Symptoms of IBD include persistent diarrhea, abdominal pain, rectal bleeding or bloody stools, in addition to weight reduction and fatigue. In the United States, about 1 in 100 adults have IBD.
The latest research sheds light on a vital genetic pathway controlled by a gene enhancer called ETS2, which is present in 95% of individuals with IBD. The researchers found that these genetic aspects increased harmful levels of inflammation within the tissues of individuals with IBD.
The results were published this week within the journal Natureare based on laboratory experiments and would must be replicated by further studies. In a second a part of their experiments, the researchers investigated the consequences of a gaggle of medication known to manage ETS2 in other non-inflammatory diseases. The laboratory experiments showed that the MEK inhibitors were capable of reduce inflammatory activity in experiments each on the cellular level and in intestinal samples from individuals with IBD.
“Crohn's disease and colitis are complex, lifelong diseases for which there is no cure, but research like this is helping us answer some of the big questions about their causes. The more we understand about inflammatory bowel disease, the more likely we are to be able to help patients live well with these diseases,” said Ruth Wakeman, Director of Services, Advocacy and Evidence at Crohn's & Colitis UK, in an announcement. “This research is a really exciting step towards a world that is one day free of Crohn's disease and colitis.”
