Crohn’s disease is a chronic and often debilitating condition that causes inflammation of the digestive system and gut. It leaves sufferers in a constant cycle of relapse and remission of symptoms that include malnutrition, abdominal pain and fatigue. With it affecting at least 115,000 people in the UK alone and up to 80 per cent of sufferers experiencing hospitalisation at some point, Crohn’s disease is a pressing healthcare issue.
Currently, there is no cure. There are only treatments to prolong periods of symptomatic relief. However, not one treatment works for all. It is a highly personal disease with varying location and severity between patients.
The Leona M. and Harry B. Hemsley Charitable Trust’s Crohn’s Disease program are funding research to address the unmet medical needs of people with the disorder. Their aim is to improve the quality of life of patients and ultimately find a cure. Based in the US, it has awarded the University of Edinburgh 1.8 million pounds to investigate the role mitochondria plays in the progression of Crohn’s disease.
Mitochondria are found in all our cells, providing them with energy (ATP) for growth and function. One theory believes that they evolved from bacteria around 2-3bn years ago, retaining their own DNA that is still independent from the nucleus.
[The Leona M. and Harry B. Hemsley haritable Trust’s Crohn’s Disease program] has awarded the University of Edinburgh 1.8 million pounds to investigate the role mitochondria plays in the progression of Crohn’s disease
When our cells are damaged, their contents, including mitochondrial DNA (mtDNA) are released into the surrounding area. In inflammatory bowel diseases (IBD), such as Crohn’s disease, it has been shown that during a relapse, the damaged cells of the gut release mtDNA. The mtDNA is then recognised as a bacterial infection by Toll-like receptor 9 (TLR9) found on the surface of circulating immune cells. This interaction has shown to trigger the immune system of the patient to attack its own tissue, ultimately promoting more inflammation and damage in the digestive tract and gut.
Investigating models of IBD disease in active human IBD and colitis mouse models, researchers at the University of Edinburgh found that sufferers of IBD had a significantly higher level of mtDNA circulating in their blood in comparison to healthy groups. They were then able to correlate that greater levels of mtDNA in the circulation induced an increase in the severity and activity of the disease.
From this discovery, it has been recognised that mtDNA has a promising role as a measurable marker of IBD injury. Dr Gwo-Tzer Ho of the University of Edinburgh’s Centre of Inflammation Research who is leading the study is taking his group’s findings further by focusing on developing mtDNA as a non-invasive test. Hopefully, removing the need for patients to undergo the current invasive procedure – a colonoscopy – for diagnosis and monitoring.
The research group hopes that by either taking a blood or stool sample of the patient and measuring their mtDNA content, doctors will be provided with information about the subtype and progression of Crohn’s disease easily. This, in turn, could provide the opportunity for patients that are experiencing an active flare-up or those with little to no healing of the bowel after treatment to receive a treatment plan that is personalised to their case.
[…] it has been recognised that mtDNA has a promising role as a measurable marker of IBD injury
Dr Gwo-Tzer Ho has said “I am honoured to receive this award, which is a reflection on the team’s efforts to understand the role of mitochondria in IBD. We are very hopeful that our work will lead to better tools to predict how the disease affects patients, which could ultimately lead to improvements in their treatment and quality of life.”
This post was written by Olivia Matthews and edited by Karolina Zieba.
