Enterohemorrhagic Escherichia coli induced hemolytic uremic syndrome and cytokine

Abstract

Enterohemorrhagic Escherichia coli (EHEC) produce Shiga toxins (STx). These toxins not only can induce cell death by inhibition of protein synthesis but also implicate a role for activation of proinflammatory cytokines and chemokines. These cytokines and chemokines can enhance STx induced cytotoxicity by enhancement of the expression of globotriaosylceramide (Gb3), the receptor of STx. Furthermore, these cytokines induce inflammatory cells infiltration. In this way, proinflammatory cytokines play an important role in the pathogenesis of EHEC infection and development of severe complications, including hemolytic uremic syndrome (HUS) and encephalopathy. It is desired to establish a monitoring system with useful clinical markers for predicting severe clinical outcomes in patients with HUS. In this review, I introduce our studies for clinical significance of serum cytokine profiles in HUS and clinical usefulness of apheresis therapy for HUS.