Cytokines expression from altered motor thalamus and behavior deficits following sublethal administration of Shiga toxin 2a involve the induction of the globotriaosylceramide receptor.

Encephalopathy associated with hemolytic uremic syndrome is produced by enterohemorrhagic E. coli (EHEC) infection, which releases the virulence factors Shiga toxin (Stx) and lipopolysaccharide (LPS). Neurological compromise is a poor prognosis and mortality factor of the disease, and the thalamus is one of the brain areas most frequently affected.

Anti-inflammatory agents reduce microglial response, demyelinating process and neuronal toxin uptake in a model of encephalopathy produced by Shiga Toxin 2.

Infections by Enterohemorrhagic Escherichia coli may cause in addition to hemolytic uremic syndrome neurological disorders which may lead to fatal outcomes in patients. The brain striatum is usually affected during this outcome. The aim of this study was to determine in this area the role of the microglia in pro-inflammatory events that may occur during Shiga toxin 2 intoxication and consequently to this, whether oligodendrocytes were being affected.