ArticlePloS one2013
Action of shiga toxin type-2 and subtilase cytotoxin on human microvascular endothelial cells.
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 32 papers, 1 of them a synthesis that pooled it.
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Who cites it
32 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.
- Glioblastoma cells potentiate the induction of the Th1-like profile in phosphoantigen-stimulated γδ T lymphocytes.Journal of neuro-oncology · 2021Pooled it
- Recombinant Human Fab Antibodies Differentially Neutralize Shiga Toxin in Renal Epithelial and Endothelial Cells.Toxins · 2026Article
- Eliglustat prevents acute kidney injury caused by Shiga toxin 2 in lethal and sublethal rat models of hemolytic uremic syndrome.Frontiers in pharmacology · 2026Article
- Pharmacological Management of Atypical Hemolytic Uremic Syndrome in Pediatric Patients: Current and Future.Paediatric drugs · 2023Article
- Diagnosis and Treatment for Shiga Toxin-ProducingToxins · 2022Review
- EnterohemorrhagicInternational journal of molecular sciences · 2022Review
- Eliglustat prevents Shiga toxin 2 cytotoxic effects in human renal tubular epithelial cells.Pediatric research · 2022Article
- Therapeutic Antibodies Against Shiga Toxins: Trends and Perspectives.Frontiers in cellular and infection microbiology · 2022Review
- The Deleterious Effects of Shiga Toxin Type 2 Are Neutralized In Vitro by FabF8:Stx2 Recombinant Monoclonal Antibody.Toxins · 2021Article
- Combined Action of Shiga Toxin Type 2 and Subtilase Cytotoxin in the Pathogenesis of Hemolytic Uremic Syndrome.Toxins · 2021Article
- Genomic Epidemiology of Shiga Toxin-ProducingAnimals : an open access journal from MDPI · 2021Article
- Review
- Human Glomerular Endothelial Cells Treated With Shiga Toxin Type 2 Activate γδ T Lymphocytes.Frontiers in cellular and infection microbiology · 2021Article
- Article
- Article
- Article
- Recent Advances in Shiga Toxin-ProducingMicroorganisms · 2018Review
- Genetic Analysis of Virulence Potential ofFrontiers in microbiology · 2018Article
- Article
- Interaction of factor H-binding protein of Streptococcus suis with globotriaosylceramide promotes the development of meningitis.Virulence · 2017Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The hemolytic uremic syndrome (HUS) associated with diarrhea is a complication of Shiga toxin (Stx)-producing Escherichia coli (STEC) infection. In Argentina, HUS is endemic and responsible for acute and chronic renal failure in children younger than 5 years old. The human kidney is the most affected organ due to the presence of very Stx-sensitive cells, such as microvascular endothelial cells. Recently, Subtilase cytotoxin (SubAB) was proposed as a new toxin that may contribute to HUS pathogenesis, although its action on human glomerular endothelial cells (HGEC) has not been described yet. In this study, we compared the effects of SubAB with those caused by Stx2 on primary cultures of HGEC isolated from fragments of human pediatric renal cortex. HGEC were characterized as endothelial since they expressed von Willebrand factor (VWF) and platelet/endothelial cell adhesion molecule 1 (PECAM-1). HGEC also expressed the globotriaosylceramide (Gb3) receptor for Stx2. Both, Stx2 and SubAB induced swelling and detachment of HGEC and the consequent decrease in cell viability in a time-dependent manner. Preincubation of HGEC with C-9 -a competitive inhibitor of Gb3 synthesis-protected HGEC from Stx2 but not from SubAB cytotoxic effects. Stx2 increased apoptosis in a time-dependent manner while SubAB increased apoptosis at 4 and 6 h but decreased at 24 h. The apoptosis induced by SubAB relative to Stx2 was higher at 4 and 6 h, but lower at 24 h. Furthermore, necrosis caused by Stx2 was significantly higher than that induced by SubAB at all the time points evaluated. Our data provide evidence for the first time how SubAB could cooperate with the development of endothelial damage characteristic of HUS pathogenesis.
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