Normal Human Gut Bacteria May Inhibit Shiga Toxin Development Following Infection With E. Coli O157:H7

Enterohemorrhagic E. coli O157:H7 causes food-borne disease with symptoms ranging from diarrhea and hemorrhagic colitis to potentially fatal hemolytic-uremic syndrome. Stx2 is released in the gut following oral ingestion of E. coli O157:H7 and is the main virulence factor responsible for the more serious complications from the disease. Despite what researchers already know about the role of Stx2 in the progression of the disease, how the molecules released by the normal intestinal bacteria impact Stx2 is largely unknown.

In the study Stx2 synthesis was analyzed following the growth of E. coli O157:H7 in contents collected from the large bowel of rats colonized with normal human intestinal bacteria. Results showed that extracellular molecules, produced in part by Bacteroides thetaiotaomicron (a predominant species of the normal human intestine), repressed Stx2 development.

"Our findings demonstrate for the first time the regulatory activity of a soluble factor produced by the complex human digestive microbiota on a bacterial virulence factor in a physiologically relevant context," say the researchers.