PhD candidate Peter Prendergast has found a celiac disease signature in gut bacteria composition.
Riddet Institute PhD candidate Peter Prendergast has just published a study revealing a gut microbiome signature of celiac disease, finding clear differences in intestinal bacterial communities in healthy people, people pre-disease onset and in sufferers with active disease.
The study was published by Mr Prendergast, along with seven co-researchers, in the academic journal Communications Medicine last month. It is research that forms part of his PhD thesis, through the University of Canterbury.
The Canterbury region in Aotearoa New Zealand is among the highest in the world for prevalence of celiac disease, with rates of more than one in 82 people.
The research reviewed multiple global investigations profiling the gut microbiome in people with and without symptoms of the disease. It found subtle but consistent changes in specific bacteria present in the small intestine and stool samples of celiac disease sufferers.
“Until this study, it was only fragmented evidence. We had some bacteria that we found changed across multiple cohorts that were hypothesised to be most likely involved. And then we had ones that weren’t consistently changed as well,” Mr Prendergast says.
The meta-analysis employed innovative computer-assisted techniques and machine learning to review vast datasets of research from around the world. It focused on consistent patterns across different stages of the disease, pinpointing particular sub-species of bacteria.
“Some people didn’t actually have celiac disease yet. They might have a relative or something like that, which makes them a high risk. And then [researchers] follow them, they sample them before they were actually diagnosed, and then they follow them for up to two years or even longer in some of these studies," Mr Prendergast says.
Evidence emerged that rates of beneficial fibre-loving butyrate bacteria and protective metabolites were high in healthy individuals, and problematic bacteria was low. Conversely, some pathogenic species of Bacteroides bacteria were increased in the digestive systems of those with celiac disease, and protective species were depleted.
These changes in bacteria communities were also observed at lower levels in individuals that went on to have celiac disease symptoms but had no active disease during testing.
“It gives us evidence that changes are happening in the gut before disease is occurring,” he says.
The changes persisted on a gluten-free diet, a diet which may diminish good bacteria further due to its reduced fibre content.
Celiac disease is an autoimmune condition triggered by eating gluten in foods. Mr Prendergast says although 30 to 40 per cent of the population carry a genetic disposition towards the disease, it affects only one to three per cent of the global population. The rate is increasing, however. The only treatment for the incurable condition is life-long adherence to a gluten-free diet.
He says the large gap between genetic disposition and disease incidence indicates environmental or dietary patterns have a part to play in the onset of disease.
“There is a huge non-genetic element to it. So that’s why we are starting to look at diet.”
Researchers believe learning more about the complex ecosystem of the gut is key to finding a way to prevent or cure the disease. Mr Prendergast says future treatments may need to focus on restoring healthy gut bacteria. Promising work involves re-introducing good bacteria that can help digest gluten in the gut, or disrupting the disease pathway by including more fibre into the diet before disease onset.
“We know from lots of microbiome studies that you can change your microbiome.”
He says the gut microbiome is very sensitive to inflammation and researchers are not sure which is most influential: antibiotic medicines, infections, diet, or a combination of things.
“There are a large number of people on a gluten-free diet who are not recovering quickly. If we could make some changes to provide some real benefit to people, and also identifying the changes we see in the prospective children holds promise that maybe one day we could find a pathway that could stop people developing the disease, or reduce its severity,” Mr Prendergast says.
A research paper by Mr Prendergast and his co-researchers, looking at a cohort of children from Canterbury, was published in Frontiers in Microbiology journal in July.
“We did see quite a unique difference in composition. The Canterbury children had quite a unique typology to the microbiome.”
Mr Prendergast says the next step would be to do further fibre metabolite research on active disease sufferers in Canterbury, where he is based, to see if the changes lead to disease. Mouse model studies investigating if it was possible to influence disease progression were also a possibility.
The original study was funded by the Health Research Council of New Zealand, with the funders having no role in the study design, data collection and analysis.
The Riddet Institute is a New Zealand Centre of Research Excellence focusing on advanced food research, hosted by Massey University in Palmerston North.
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