Journal
JOURNAL OF INFECTIOUS DISEASES
Volume 198, Issue 9, Pages 1398-1406Publisher
OXFORD UNIV PRESS INC
DOI: 10.1086/591911
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Funding
- NHLBI NIH HHS [HL77378, R01 HL044455, HL44455, HL 44455, R01 HL044455-18] Funding Source: Medline
- NIAID NIH HHS [R01 AI024431-22, AI024431, R01 AI024431, T32 AI055432] Funding Source: Medline
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Affinity-purified Shiga toxin (Stx) 2 given intraperitoneally to mice caused weight loss and hind-limb paralysis followed by death. Globotriaosylceramide (Gb3), 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 Gb3 in neurons and endothelial cells. Mouse Gb3 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.
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