ArticleInfection and immunity2013
Shiga toxin 2 reduces complement inhibitor CD59 expression on human renal tubular epithelial and glomerular endothelial cells.
Article in Infection and immunity, 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, 44 citations in OpenAlex.
- Neutrophil Extracellular Traps Aggravate Injury in Complement-Mediated Thrombotic Microangiopathy.Journal of the American Society of Nephrology : JASN · 2026Article
- Molecular determinants of STEC-HUS: from complement activation to microvascular thrombosis.Frontiers in immunology · 2026Article
- The Role of the Complement System in the Pathogenesis of Infectious Forms of Hemolytic Uremic Syndrome.Biomolecules · 2023Review
- HUS with mutations in CFH and STEC infection treated with eculizumab in a 4-year-old girl.Pediatric nephrology (Berlin, Germany) · 2023Article
- Diagnosis and Treatment for Shiga Toxin-ProducingToxins · 2022Review
- Stx2 Induces Differential Gene Expression and Disturbs Circadian Rhythm Genes in the Proximal Tubule.Toxins · 2022Article
- Article
- Cell Biological Responses after Shiga Toxin-1 Exposure to Primary Human Glomerular Microvascular Endothelial Cells from Pediatric and Adult Origin.International journal of molecular sciences · 2021Article
- Review
- Article
- Shiga Toxin 2a Binds to Complement Components C3b and C5 and Upregulates Their Gene Expression in Human Cell Lines.Toxins · 2020Article
- Molecular Biology ofToxins · 2020Review
- C3 levels and acute outcomes in Shiga toxin-related hemolytic uremic syndrome.Pediatric nephrology (Berlin, Germany) · 2020Article
- Low C3 Serum Levels Predict Severe Forms of STEC-HUS With Neurologic Involvement.Frontiers in medicine · 2020Article
- Eculizumab in the treatment of Shiga toxin haemolytic uraemic syndrome.Pediatric nephrology (Berlin, Germany) · 2019Review
- Shiga toxin triggers endothelial and podocyte injury: the role of complement activation.Pediatric nephrology (Berlin, Germany) · 2019Review
- Complement Activation Contributes to the Pathophysiology of Shiga Toxin-Associated Hemolytic Uremic Syndrome.Microorganisms · 2019Review
- Complement activation is associated with more severe course of diarrhea-associated hemolytic uremic syndrome, a preliminary study.European journal of pediatrics · 2018Article
- Carboxypeptidase B2 and N play different roles in regulation of activated complements C3a and C5a in mice.Journal of thrombosis and haemostasis : JTH · 2018Article
- CFH gene mutation in a case of Shiga toxin-associated hemolytic uremic syndrome (STEC-HUS).Pediatric nephrology (Berlin, Germany) · 2016Article
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Authors and funding
10 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Infections with enterohemorrhagic Escherichia coli (EHEC) are a primary cause of hemolytic-uremic syndrome (HUS). Recently, Shiga toxin 2 (Stx2), the major virulence factor of EHEC, was reported to interact with complement, implying that the latter is involved in the pathogenesis of EHEC-induced HUS. The aim of the present study was to investigate the effect of Stx2 on the expression of membrane-bound complement regulators CD46, CD55, and CD59 on proximal tubular epithelial (HK-2) and glomerular endothelial (GEnC) cells derived from human kidney cells that are involved in HUS. Incubation with Stx2 did not influence the amount of CD46 or CD55 on the surface of HK-2 and GEnC cells, as determined by fluorescence-activated cell sorter analysis. In contrast, CD59 was significantly reduced by half on GEnC cells, but the reduction on HK-2 cells was less pronounced. With increasing amounts of Stx2, reduction of CD59 also reached significance in HK-2 cells. Enzyme-linked immunosorbent assay analyses showed that CD59 was not present in the supernatant of Stx2-treated cells, implying that CD59 reduction was not caused by cleavage from the cell surface. In fact, reverse transcription-quantitative PCR analyses showed downregulation of CD59 mRNA as the likely reason for CD59 cell surface reduction. In addition, a significant increase in terminal complement complex deposition on HK-2 cells was observed after treatment with Stx2, as a possible consequence of CD59 downregulation. In summary, Stx2 downregulates CD59 mRNA and protein levels on tubular epithelial and glomerular endothelial cells, and this downregulation likely contributes to complement activation and kidney destruction in EHEC-associated HUS.
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