Bacteria that reside in human gut may trigger autoimmune reactions by producing human-like proteins that mimic a naturally occurring and crucial cell protein.
Researchers at Queen’s University Belfast in Ireland report that patients with autoimmune disorders — such as multiple sclerosis (MS), rheumatoid arthritis, and ulcerative colitis — have higher-than-normal levels of a “mimic protein” produced by Bacteroides fragilis – a member of the gut microbiome in people.
This protein has the potential to activate the immune system to attack not only the bacteria-produced protein, but also the natural protein by mistake, contributing to autoimmune deregulation.
The finding was reported in the study “Antigenic mimicry of ubiquitin by the gut bacterium Bacteroides fragilis: a potential link with autoimmune disease,” published in the journal Clinical and Experimental Immunology.
Several studies in recent years have demonstrated that gut resident bacteria play an important role in regulating the immune system and its responses. Some suggest that the gut microbiome can work to protect against MS, while others report that gut bacteria can actually contribute to disease progression.
Despite the contradictory results, these studies inspired work to better understand the underlying mechanisms of autoimmunity, and to potentially develop strategies to treat serious autoimmune disorders such as MS.
The Belfast researchers found another possible culprit for immune system deregulation and induced autoimmunity, the common gut bacteria Bacteroides fragilis. These bacteria were found to produce a protein called BfUbb that is 63% identical to the naturally produced ubiquitin protein, which is central to cell processes.
“When we mapped the genome of Bacteroides fragilis a few years ago we were astonished to discover a human-like gene not present in any other bacteria. The protein produced from this gene is nearly the same shape as a protein in almost every human cell,” Sheila Patrick, PhD, a professor at Queen’s University and the study’s senior author, said in a university news release.
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