Other evidence that supports a pathogenic role for EspP in D+HUS includes cleavage of human apolipoprotein A-I [26], which acts as a stabilizing factor for prostacyclin (PGI2) [27], an inhibitor of platelet activation [28]; downregulation of complement activation by cleavage of C3/C3b and C5 which may facilitate adherence [29] and colonization of the EHEC in the gut by protecting the bacteria from opsonization and complement-mediated lysis [30]; and EspP forming rope-like fibers with cytopathic and adhesive properties [31]. Here, APOA1 is linked to atypical hemolytic-uremic syndrome.