A New York City research team believes that clinical SLE disease is associated with microbiome imbalances, specifically with decreases in the diversity and blooms of specific operational taxonomic units in the intestine.
Systemic lupus erythematosus (SLE) is caused by a combination of genetic and environmental factors. A team of researchers from New York City believes that clinical SLE disease is associated with microbiome imbalances, specifically with decreases in the diversity and blooms of specific operational taxonomic units in the the intestine.
In an abstract presented at the 2015 American College of Rheumatology Annual Meeting in San Francisco, CA, Greg Silverman, MD, and colleagues at the NYU School of Medicine noted that animal models in other studies of inflammatory and autoimmune disease have shown intestinal bacteria play a role in the development of these tissues.
They looked at a group of 67 SLE adult patients and 16 healthy controls, analyzing bacteria in fecal samples.
They found the patients with SLE had microbiota that were less diverse. SLE patients displayed a significant increase in Proteobacteria and a decrease in Firmicutes.
Also, the SLE patients had increased representation of specific operational taxonomic units. "Interestingly the anaerobic species Prevotella copri, recently linked to new-onset RA, was expanded in a subset of SLE patients but not in healthy controls," they noted.
The differences in patients' microbes were not related to use of medications by the SLE patients, the researchers said.
"Studies of the intestinal bacteria coated with IgA highlighted that only microbes of certain genera and OTU are immunologically recognized by the lupus host," they wrote, adding, "We speculate that these candidate pathobiont species may act as triggers for disease initiation and flares."