Infection with Shiga toxin-producing Escherichia coli (STEC) may cause hemorrhagic
colitis, hemolytic uremic syndrome (HUS) and encephalopathy. The mortality rate derived from
HUS adds up to 5% of the cases, and up to 40% when the central nervous system (CNS) is involved.
In addition to the well-known deleterious effect of Stx, the gram-negative STEC releases
lipopolysaccharides (LPS) and may induce a variety of inflammatory responses when released in
the gut. Common clinical signs of severe CNS injury include sensorimotor, cognitive, emotional
and/or autonomic alterations. In the last few years, a number of drugs have been experimentally
employed to establish the pathogenesis of, prevent or treat CNS injury by STEC. The strategies in
these approaches focus on: 1) inhibition of Stx production and release by STEC, 2) inhibition of Stx
bloodstream transport, 3) inhibition of Stx entry into the CNS parenchyma, 4) blockade of deleterious
Stx action in neural cells, and 5) inhibition of immune system activation and CNS inflammation.
Fast diagnosis of STEC infection, as well as the establishment of early CNS biomarkers of
damage, may be determinants of adequate neuropharmacological treatment in time.
Keywords: Neurodegeneration, neuroprotection, neuropharmacology, reactive astrocytes, microvasculature, oligodendrocytes,
microglial cells, Shiga toxin 2, images, brain, cerebellum, transmission electron microscopy, fluorescence microscopy,
lipopolysaccharides, inflammation, Hemolytic Uremic Syndrome.
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