24 research outputs found
Genome sequencing and comparative genomics provides insights on the evolutionary dynamics and pathogenic potential of different H-serotypes of Shiga toxin-producing Escherichia coli O104
Affinity-Based Screening of Tetravalent Peptides Identifies Subtype-Selective Neutralizers of Shiga Toxin 2d, a Highly Virulent Subtype, by Targeting a Unique Amino Acid Involved in Its Receptor Recognition
The Evasive Enemy: Insights into the Virulence and Epidemiology of the Emerging Attaching and Effacing Pathogen Escherichia albertii
Zebrafish embryo sensitivity test as in vivo platform to anti-Shiga toxin compound screening
Culture‐positive shigellosis cases are epidemiologically different to culture‐negative/PCR‐positive cases
Shiga toxin 2 affects the central nervous system through receptor globotriaosylceramide localized to neurons
Affinity-purified Shiga toxin (Stx) 2 given intraperitoneally to mice caused weight loss and hind-limb paralysis followed by death. Globotriaosylceramide (Gb(3)), the receptor for Stx2, was localized to neurons of the central nervous system (CNS) of normal mice. Gb3 was not found in astrocytes or endothelial cells of the CNS. In human cadaver CNS, we found Gb(3) in neurons and endothelial cells. Mouse Gb(3) localization was confirmed by immunoelectron microscopy. In Stx2-exposed mice, anti-Stx2-gold immunoreaction was positive in neurons. During paralysis, after Stx2 injection, multiple glial nuclei were observed surrounding motoneurons by electron microscopy. Also revealed was a lamellipodia-like process physically inhibiting the synaptic connection of motoneurons. Ca2+ imaging of cerebral astrocytic end-feet in Stx2-treated mouse brains suggested that the toxin increased neurotransmitter release from neurons. In this article, we propose that the neuron is a primary target of Stx2, affecting neuronal function and leading to paralysis