This knowledge could potentially lead to new and more successful treatments to prevent these flares, they added.
These recurrent bouts of systemic lupus erythematosus, where the body’s immune systems attacks its own tissues, were strongly linked with blooms of the gut bacterium Ruminococcus blautia gnavus.
The team from New York University Gross School of Medicine saw these bacterial blooms at the same time as disease flare-ups in five of 16 women with lupus over a four-year period.
Study participants were patients at NYU Langone who were closely monitored for disease flare-ups and compared to 22 female volunteers of similar age and racial background who were healthy and did not have lupus.
“Our findings provide the strongest evidence to date that silent growths of Ruminococcus blautia gnavus are tied to active serious renal disease in lupus patients,” said lead investigator Doua Azzouz, a postdoctoral researcher in the department of medicine at NYU Langone Health.
“Interestingly, our study also established this common bacterial link among a racially diverse group of females with varying forms of lupus,” she said in an NYU news release.
Lupus causes damaging inflammation in the joints, skin, blood vessels and especially in the kidneys, affecting about 1.5 million Americans. It affects more women than men and more Black, Hispanic and Asian Americans than white people.
About half of patients develop lupus nephritis. Among those, one-quarter are likely to experience end-stage renal disease that may require regular dialysis and even kidney transplantation.
Four of the women studied with these bacteria blooms had severe cases of the most common and kidney-specific form of the disease, lupus nephritis. One of the patients had a severe example of lupus involving inflammation in multiple joints.
The researchers identified 34 genes that already had established links to the bacterium’s growth in people with inflammation. Experts suspect bacterial imbalances trigger genetic factors that cause lupus.
Researchers also looked at how tightly these patients’ immune system antibodies bonded to the bacteria, as they would do to an invading virus.
They saw a strong affinity between these antibodies and bacterial lipoglycan molecules that are known triggers of inflammation. The researchers noted that these lipoglycans were common in R. gnavus strains in lupus patients, but not in healthy people.
“Our goal is to use our growing understanding of the biological pathways that underpin the disease to develop new treatments that prevent or treat flares for all forms of lupus,” said senior investigator and immunologist Dr. Gregg Silverman, a professor of internal medicine in the departments of medicine and pathology at NYU Langone.
“Such future treatments for lupus, especially lupus nephritis, could potentially decrease the use of drugs designed to dampen the immune system and instead promote the use of less toxic antibacterial agents, probiotics or dietary regimens that prevent imbalances such as Ruminococcal blooms in the local gut bacterial population, or microbiome,” Silverman said in the release.
Other areas of research could include experiments to see how R. gnavus colonization triggers lupus in mice.
The U.S. National Institutes of Health provided some of the funding for the research, which was published online June 27 in the Annals of Rheumatic Diseases.
The U.S. National Institutes of Health has more on lupus.
SOURCE: NYU Grossman School of Medicine, news release, June 27, 2023
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