ArticleThe American journal of pathology2013
Distinct renal pathology and a chemotactic phenotype after enterohemorrhagic Escherichia coli shiga toxins in non-human primate models of hemolytic uremic syndrome.
Article in The American journal of pathology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 43 citations in OpenAlex.
- Monocytes serve as Shiga toxin carriers during the development of hemolytic uremic syndrome.Cellular & molecular biology letters · 2025Article
- Shiga Toxin: Emerging Producer Strains, Prophylactic Approaches, and Application in Cancer Therapy.Journal of cancer prevention · 2024Review
- Shiga Toxins Produced by EnterohaemorrhagicJournal of microbiology and biotechnology · 2024Article
- Article
- Review
- Article
- Roles of Shiga Toxins in Immunopathology.Toxins · 2019Review
- Pathogenic role of inflammatory response during Shiga toxin-associated hemolytic uremic syndrome (HUS).Pediatric nephrology (Berlin, Germany) · 2018Review
- Dextran Sulfate Sodium Colitis Facilitates Colonization with Shiga Toxin-Producing Escherichia coli: a Novel Murine Model for the Study of Shiga Toxicosis.Infection and immunity · 2018Article
- Modeling Hemolytic-Uremic Syndrome: In-Depth Characterization of Distinct Murine Models Reflecting Different Features of Human Disease.Frontiers in immunology · 2018Article
- Article
- Shiga Toxin Therapeutics: Beyond Neutralization.Toxins · 2017Review
- Review
- Do the A subunits contribute to the differences in the toxicity of Shiga toxin 1 and Shiga toxin 2?Toxins · 2015Review
- Effects of Shiga toxin type 2 on a bioengineered three-dimensional model of human renal tissue.Infection and immunity · 2015Article
- Pro-Coagulant Endothelial Dysfunction Results from EHEC Shiga Toxins and Host Damage-Associated Molecular Patterns.Frontiers in immunology · 2015Article
- Natural killer T (NKT) cells accelerate Shiga toxin type 2 (Stx2) pathology in mice.Frontiers in microbiology · 2015Article
- Direct acute tubular damage contributes to Shigatoxin-mediated kidney failure.The Journal of pathology · 2014Article
- Complement, thrombotic microangiopathy and disseminated intravascular coagulation.Journal of intensive care · 2014Review
- Shiga toxins expressed by human pathogenic bacteria induce immune responses in host cells.Journal of microbiology (Seoul, Korea) · 2013Review
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Enterohemorrhagic Escherichia coli cause approximately 1.5 million infections globally with 176,000 cases occurring in the United States annually from ingesting contaminated food, most frequently E. coli O157:H7 in ground beef or fresh produce. In severe cases, the painful prodromal hemorrhagic colitis is complicated by potentially lethal hemolytic uremic syndrome (HUS), particularly in children. Bacterial Shiga-like toxins (Stx1, Stx2) are primarily responsible for HUS and the kidney and neurologic damage that ensue. Small animal models are hampered by the inability to reproduce HUS with thrombotic microangiopathy, hemolytic anemia, and acute kidney injury. Earlier, we showed that nonhuman primates (Papio) recapitulated clinical HUS after Stx challenge and that novel therapeutic intervention rescued the animals. Here, we present detailed light and electron microscopic pathology examination of the kidneys from these Stx studies. Stx1 challenge resulted in more severe glomerular endothelial injury, whereas the glomerular injury after Stx2 also included prominent mesangiolysis and an eosinophilic inflammatory infiltration. Both toxins induced glomerular platelet-rich thrombi, interstitial hemorrhage, and tubular injury. Analysis of kidney and other organs for inflammation biomarkers showed a striking chemotactic profile, with extremely high mRNA levels for IL-8, monocyte chemoattractant protein 1, and macrophage inflammatory protein 1α and elevated urine chemokines at 48 hours after challenge. These observations give unique insight into the pathologic consequences of each toxin in a near human setting and present potential pathways for therapeutic intervention.
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