Bacterial exposure has been identified as a potential environmental risk factor in developing celiac disease, a hereditary autoimmune-like condition that affects about one in 70 Australians.
It is estimated that half of all Australians are born with one of two genes that cause celiac disease, and approximately one in 40 are likely to develop the condition.
People with celiac disease must follow a lifelong gluten-free diet, as even small amounts of gluten can cause health problems.
While environmental factors are known to trigger Celiac Disease in those with the genetic predisposition, exactly how that works has remained unclear.
Scientists from the Monash Biomedicine Discovery Institute (BDI) and ARC Center of Excellence in Advanced Molecular Imaging, have now provided a molecular foundation for microbial exposure as a potential environmental factor in the development of celiac disease.
The results of the study, done in collaboration with researchers at Leiden University Medical Center and the Walter and Eliza Hall Institute of Medical Research, have been published in the journal Nature Structural and Molecular Biology.
Co-Lead researcher Dr. Hugh Reid, from Monash University, said the team showed, at the molecular level, how receptors isolated from immune T cells from celiac disease patients can recognize 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, he said.
“In celiac 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,” he said.
“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 said the findings could eventually lead to diagnostic or therapeutic approaches to celiac disease.
Reference: “T cell receptor cross-reactivity between gliadin and bacterial peptides in celiac disease” by Jan Petersen, Laura Ciacchi, Mai T. Tran, Khai Lee Loh, Yvonne Kooy-Winkelaar, Nathan P. Croft, Melinda Y. Hardy, Zhenjun Chen, James McCluskey, Robert P. Anderson, Anthony W. Purcell, Jason A. Tye-Din, Frits Koning, Hugh H. Reid and Jamie Rossjohn, 23 December 2019, Nature Structural & Molecular Biology.
About celiac disease
Celiac disease is caused by an aberrant reaction of the immune system to gluten, a protein that occurs naturally in grains such as wheat, rye, barley, and oats, and therefore 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.
In patients with CD, activation of these T cells leads to an inflammatory response in the small intestine causing a wide range of symptoms including diarrhea, bloating, and malabsorption of nutrients, to name a few.
People with celiac disease must follow a lifelong gluten-free diet, as even small amounts of gluten can cause health problems. If left untreated, the disease can cause serious issues including malnutrition, osteoporosis, depression, and infertility, and there is a small increased risk of certain forms of cancer, such as lymphoma of the small bowel.