ArticlePloS one2013
Investigation of encephalopathy caused by Shiga toxin 2c-producing Escherichia coli infection in mice.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
8 citing papers in PubMed, 23 citations in OpenAlex.
- Shiga Toxin-ProducingKidney international reports · 2025Article
- Effects of Muse Cell on a Mouse Model With Acute Encephalopathy.Brain and behavior · 2025Article
- Diagnosis and Treatment for Shiga Toxin-ProducingToxins · 2022Review
- Streptococcal meningitis reveals the presence of residual streptococci and down-regulated aquaporin 4 in the brain.Archives of microbiology · 2021Article
- Identification of Antibiotics That Diminish Disease in a Murine Model of Enterohemorrhagic Escherichia coli Infection.Antimicrobial agents and chemotherapy · 2020Article
- Rescue from Stx2-Producing E. coli-Associated Encephalopathy by Intravenous Injection of Muse Cells in NOD-SCID Mice.Molecular therapy : the journal of the American Society of Gene Therapy · 2020Article
- Pathogenic role of inflammatory response during Shiga toxin-associated hemolytic uremic syndrome (HUS).Pediatric nephrology (Berlin, Germany) · 2018Review
- Role of Shiga/Vero toxins in pathogenesis.Microbiology spectrum · 2014Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A large outbreak of Shiga toxin (Stx)-producing enteroaggregative Escherichia coli (EAEC) O104:H4 occurred in northern Germany. From this outbreak, at least 900 patients developed hemolytic uremic syndrome (HUS), resulting in more than 50 deaths. Thirty percent of the HUS patients showed encephalopathy. We previously established a mouse model with encephalopathy associated with blood brain barrier (BBB) damage after oral infection with the Shiga toxin (Stx) 2c-producing Escherichia coli O157: H- strain E32511 (E32511). In this model, we detected high expression of the Stx receptor synthase enzyme, glycosphingolipid globotriaosylceramide (Gb3) synthase, in endothelial cells (ECs) and neurons in the reticular formation of the medulla oblongata by in situ hybridization. Caspase-3 was activated in neurons in the reticular formation of the medulla oblongata and the anterior horn of the spinal cord. Astrocytes (ASTs) were activated in the medulla oblongata and spinal cord, and a decrease in aquaporin 4 around the ECs suggested that BBB integrity was compromised directly by Stx2c or through the activation of ASTs. We also report the effectiveness of azithromycin (AZM) in our model. Moreover, AZM strongly inhibited the release of Stx2c from E32511 in vitro.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.