New research has uncovered how a dietary intervention could help prevent the development of the autoimmune disease, systemic lupus erythematosus (SLE). Using mouse models of lupus, the team from Yale University set out to test the role of diet and the microbiota and dissect its mechanisms as the role of commensal bacteria in autoimmunity remains unclear.
“We dissected, molecularly, how diets can work on the gut microbiome,” said senior author Martin Kriegel, M.D., Ph.D., associate professor adjunct in the department of immunobiology, Yale University School of Medicine. “We identified a pathway that is driving autoimmune disease and mitigated by the diet.”
The paper, A Diet-Sensitive Commensal Lactobacillus Strain Mediates TLR7-Dependent Systemic Autoimmunity was published recently in Cell Host & Microbe.
The team first identified the bacterium, Lactobacillus reuteri, in the gut of the mice that triggered an immune response leading to the disease. Specifically, in the Toll-like receptor 7 (TLR7)-dependent mouse models of lupus, L. reuteri stimulated immune cells known as dendritic cells, as well as immune system pathways that exacerbated disease development.
To investigate the potential impact of diet on the presence of this bacteria in the mice, first author Daniel Zegarra-Ruiz, a graduate student in the lab, fed the mice “resistant starch”— a diet that mimics a high-fiber diet in humans. Foods that are high in resistant starch are rice, whole grains such as oats and barley, beans, peas, and lentils.
The resistant starch is not absorbed in the small intestine but ferments in the large intestine, enriching good bacteria and causing the secretion of short-chain fatty acids. The diet suppressed both the growth and movement of L. reuteri bacteria outside the gut that would otherwise lead to autoimmune disease.