LOCAL ADMINISTRATION OF SHIGA TOXIN 2 INDUCES THE EXPRESSION OF THE GLOBOTRIAOSYLCERAMIDE (GB3) RECEPTOR IN THE RAT BRAIN

C F TIRONI FARINATI , W MORRIS, A VENZANO, J BOCCOLI , C. F. LOIDL, C IBARRA, J GOLDSTEIN

Ciudad de Buenos Aires

Simposio; 7th International Symposium on Shiga Toxin (Verocytotoxin) - Producing Escherichia coli Infections - Buenos Aires; 2009

Asociacion argentina de microbiologia

Shiga toxin-producing Escherichia coli (STEC) causes hemorrhagic diarrhea, hemolytic uremic syndrome (HUS) and various encephalopathies, one of the major risk factors of children mortality. Shiga toxin (Stx) binds to its receptor, the glycolipid globotriaosylceramide (Gb3) and produces cell death. At present, the cerebral distribution of Gb3 is a matter of controversy. We previously published that the intracerebroventricular (ICV) administration of Stx2 in the rat brain causes neuronal and glial alterations that included neuronal death (1,2). The aim of this work is to demonstrate the presence of the receptor GB3 on normal rat brains and the changes in its expression after the ICV administration of Stx2.Methods After 8 days of treatment, SD male rats were anesthetized, perfused and their brains were processed to perform double immunofluorescence confocal microscopy studies using commercial antibodies targeting Gb3, Stx2, Map2 (neuronal marker) and GFAP (astrocytic marker).Results The immunodetection of the Gb3 receptor was observed in neurons and microvessels of striatum, hippocampus, cerebral cortex and hypothalamus of rat brains after ICV administration of a vehicle. The increase in the expression of Gb3 receptor after Stx2 microinfusion were observed in neurons, microvessels and astrocytes of the same brain regions but mainly located next to the ventricle (p