What breakthrough in inflammatory bowel disease was discovered this week?

Researchers made significant progress in identifying a cause of IBD, potentially leading to improved treatment options

What is IBD?

Inflammatory bowel disease, more commonly known as IBD, is an umbrella term for Crohn’s disease and ulcerative colitis.

They arise when the immune system attacks the bowel, causing an array of debilitating symptoms from abdominal pain and weight loss to diarrhoea and blood in stools.

Amy Kelly, chief executive of Crohn’s and Colitis Ireland, a charity representing people with the disease, said although the two conditions have very similar symptoms, they affect people in different ways.

The two conditions also impact different parts of the digestive system.

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“For Crohn’s disease, the inflammation can be in any part of the digestive tract, from the mouth to the anus, while colitis is generally localised to the colon,” she added.

According to Kelly, there is no cure and sufferers have “times of a flare and times of remission”. About 40,000 people in Ireland have IBD.

Is IBD the same thing as IBS?

No, though the two often get mixed up. Although they present with very similar symptoms, IBD is a disease that is caused by inflammation or ulcers. Irritable bowel syndrome (IBS), on the other hand, is a functional condition in which contents move too fast or too slow through the intestines, usually accompanied by abdominal pain.

So, what did researchers discover?

There is very little that has been known about what causes IBD, other than it is most commonly diagnosed among young people.

However, research published in the journal Nature this week found a section of DNA that is only active in some immune cells that are known to cause inflammation in the bowels.

The researchers, from the Francis Crick Institute, working with University College London and Imperial College London, found a gene called ETS2 is central to the inflammatory behaviour of immune cells called macrophages and their ability to damage the bowel in IBD.

Why is this a good thing?

Well, a better understanding of the disease provides for increased treatment options.

The researchers highlighted in their study that there has been “limited efficacy” of available treatments, and a high failure rate during drug development – highlighting an “urgent need” to better understand the disease and how it works.

According to Kelly, some people with IBD can be on medication for the rest of their lives and might need surgery to remove part of their colon, while some might require a stoma bag.

Does the research provide for new treatment?

This study creates a glimmer of hope for improved treatment options. The researchers illustrated that this biological pathway is drug-targetable.

There are no drugs that block the gene ETS2 specifically. However, the researchers found cancer treatment drugs called MEK inhibitors switched off the inflammatory effects of the gene.

After testing, researchers observed the medication reduced inflammation in immune cells and in gut samples from patients with IBD.

However, this medication can have side effects in other organs. As a result, the researchers are working to find ways to deliver it directly to immune cells. There would need to be clinical trials before this potential treatment option could be rolled out to patients.

Christina Stankey, PhD student at the Crick Institute, and co-first author of the research, said IBD and other autoimmune conditions are “really complex, with multiple genetic and environmental risk factors”.

“To find one of the central pathways, and show how this can be switched off with an existing drug, is a massive step forward,” she added.