Coeliac disease linked to bacterial exposure, new study suggests

dictonary definition of gluten
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Bacterial exposure has been identified as a potential environmental risk factor in developing coeliac disease, a hereditary autoimmune-like condition that affects around 1 in 100 people in the UK and Europe.  

Although environmental factors are known to trigger coeliac disease in those with the genetic predisposition, exactly how that works has remained unclear until now.

What is coeliac disease? 

Coeliac disease is caused by an abnormal reaction of the immune system to gluten, a protein which occurs naturally in grains such as wheat, rye, barley and oats. Gluten is typically found in bread, pastries and cakes.  

Immune system cells, known as T cells, regard gluten as a foreign substance and initiate action against it. This action leads to an inflammatory response in the small intestine causing a wide range of symptoms including diarrhoea, bloating and malabsorption of nutrients, to name a few. 

People who have coeliac disease must follow a lifelong gluten-free diet, as even small amounts of gluten can cause severe health problems. If left untreated, it can cause serious issues including malnutrition, osteoporosis, depression and unexplained infertility, and there is a small increased risk of certain forms of cancer, such as lymphoma of the small bowel. 

The results of the study 

Scientists from the Monash Biomedicine Discovery Institute (BDI) and ARC Centre of Excellence in Advanced Molecular Imaging, have now provided a molecular foundation for microbial exposure as a potential environmental factor in the development of coeliac disease.  

Co-Lead researcher Dr Hugh Reid, from Monash University, Australia, explained the team showed – at the molecular level – how receptors isolated from immune T cells from coeliac disease patients can recognise protein fragments from certain bacteria that mimic those fragments from gluten. Exposure to such bacterial proteins may be involved in the generation of aberrant recognition of gluten by these same T cells when susceptible individuals eat cereals containing gluten. 

Reid said: “In coeliac disease, you get aberrant reactivity to gluten and we have provided a proof-of-principle that there’s a link between gluten proteins and proteins that are found in some bacteria. 

“That is, it’s possible that the immune system reacts to the bacterial proteins in a normal immune response and in so doing develops a reaction to gluten proteins because, to the immune system, they look indistinguishable – like a mimic.” 

Dr Reid hopes that the findings could eventually lead to diagnostic or therapeutic approaches to coeliac disease. 

The results of the study, done in collaboration with researchers at Leiden University Medical Centre and the Walter and Eliza Hall Institute of Medical Research, have been published in the journal of Nature Structural and Molecular Biology. 

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