Shiga toxin-producing Escherichia coli (STEC) is associated with hemolytic uremic syndrome (HUS). Although most clinical isolates of STEC produce hemolysin (called enterohemolysin), the precise role of enterohemolysin in the pathogenesis of STEC infections is unknown. Here we demonstrated that E. coli carrying the cloned enterohemolysin operon (hlyC, A, B, D genes) from an STEC human strain induced the production of interleukin-1β (IL-1β) through its mRNA expression but not tumor necrosis factor-α from human monocytes. No IL-1β release was observed with an enterohemolysin (HlyA)-negative, isogenic E. coli strain carrying a mutation in the hlyA gene. The data suggest that enterohemolysin, a pore-forming toxin, induces the production of IL-1β, which is one of serum risk markers for HUS.
