Gut bacteria found in the small intestines could play a role in triggering an autoimmune response in genetically predisposed individuals, such as those with lupus, a research report suggests.
Recent studies have shown that gut commensals can reside within gastrointestinal-associated lymph tissues of healthy hosts, but it has been unclear whether pathobiont translocation was involved in systemic autoimmunity. Silvio Manfredo Vieira, PhD, and his colleagues at Yale University, New Haven, Conn., addressed this knowledge gap by studying the Gram-positive gut commensal Enterococcus gallinarum, which was identified in mesenteric lymph nodes, liver, and spleen cultures from genetically susceptible mouse models.
In monocolonized and autoimmune-prone mice, the research team reported in Science that E. gallinarum could spontaneously translocate outside of the gut to lymph nodes, the liver, and spleen and initiate the production of autoantibodies and inflammation that led to death.The researchers found that they could suppress the autoimmunity with antibiotics or an intramuscular vaccine targeted at E. gallinarum. The vaccine reduced levels of serum autoantibodies, prolonged survival in the mice, and also prevented translocation, as no growth of E. gallinarum was observed in internal organs.