ReviewPediatric nephrology (Berlin, Germany)2018
Pathogenic role of inflammatory response during Shiga toxin-associated hemolytic uremic syndrome (HUS).
Review in Pediatric nephrology (Berlin, Germany), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 51 citations in OpenAlex.
- Review
- Food-borne bacterial pathogens: emerging approaches in detection and prevention.Archives of microbiology · 2026Review
- Eliglustat prevents acute kidney injury caused by Shiga toxin 2 in lethal and sublethal rat models of hemolytic uremic syndrome.Frontiers in pharmacology · 2026Article
- Antimicrobial and anti-virulent efficacies of melanin, and risk factors associated withFrontiers in cellular and infection microbiology · 2026Article
- Neutrophil extracellular traps and acute kidney injury: a narrative review.Frontiers in immunology · 2026Review
- The role of the complement system in Shiga toxin-associated hemolytic uremic syndrome.Pediatric nephrology (Berlin, Germany) · 2025Article
- Hypertriglyceridemia in STEC-hemolytic uremic syndrome: does it really matter?Pediatric nephrology (Berlin, Germany) · 2024Article
- Article
- Volume expansion mitigates Shiga toxin-producing E. coli-hemolytic uremic syndrome in children.Pediatric nephrology (Berlin, Germany) · 2024Article
- Modeling Shiga toxin-induced human renal-specific microvascular injury.Integrative biology : quantitative biosciences from nano to macro · 2024Article
- Transition from acute kidney injury to chronic kidney disease in a long-term murine model of Shiga toxin-induced hemolytic-uremic syndrome.Frontiers in immunology · 2024Article
- The diverse landscape of AB5-type toxins.Engineering microbiology · 2023Review
- Toll-like Receptor 4 in Acute Kidney Injury.International journal of molecular sciences · 2023Review
- Assessment of interleukin-10 promoter variant (-1082A/G) and cytokine production in patients with hemolytic uremic syndrome.Frontiers in pediatrics · 2023Article
- Bruton's tyrosine kinase inhibition attenuates disease progression by reducing renal immune cell invasion in mice with hemolytic-uremic syndrome.Frontiers in immunology · 2023Article
- Text Mining of Biomedical Articles Using the Konstanz Information Miner (KNIME) Platform: Hemolytic Uremic Syndrome as a Case Study.Healthcare informatics research · 2022Article
- Therapeutic Antibodies Against Shiga Toxins: Trends and Perspectives.Frontiers in cellular and infection microbiology · 2022Review
- Intestinal mucus-derived metabolites modulate virulence of a clade 8 enterohemorrhagicFrontiers in cellular and infection microbiology · 2022Article
- Hemoconcentration and predictors in Shiga toxin-producing E. coli-hemolytic uremic syndrome (STEC-HUS).Pediatric nephrology (Berlin, Germany) · 2021Article
- Severely ill pediatric patients with Shiga toxin-associated hemolytic uremic syndrome (STEC-HUS) who suffered from multiple organ involvement in the early stage.Pediatric nephrology (Berlin, Germany) · 2021Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hemolytic uremic syndrome (HUS) is defined as a triad of noninmune microangiopathic hemolytic anemia, thrombocytopenia, and acute kidney injury. The most frequent presentation is secondary to Shiga toxin (Stx)-producing Escherichia coli (STEC) infections, which is termed postdiarrheal, epidemiologic or Stx-HUS, considering that Stx is the necessary etiological factor. After ingestion, STEC colonize the intestine and produce Stx, which translocates across the intestinal epithelium. Once Stx enters the bloodstream, it interacts with renal endothelial and epithelial cells, and leukocytes. This review summarizes the current evidence about the involvement of inflammatory components as central pathogenic factors that could determine outcome of STEC infections. Intestinal inflammation may favor epithelial leakage and subsequent passage of Stx to the systemic circulation. Vascular damage triggered by Stx promotes not only release of thrombin and increased fibrin concentration but also production of cytokines and chemokines by endothelial cells. Recent evidence from animal models and patients strongly indicate that several immune cells types may participate in HUS physiopathology: neutrophils, through release of proteases and reactive oxygen species (ROS); monocytes/macrophages through secretion of cytokines and chemokines. In addition, high levels of Bb factor and soluble C5b-9 (sC5b-9) in plasma as well as complement factors adhered to platelet-leukocyte complexes, microparticles and microvesicles, suggest activation of the alternative pathway of complement. Thus, acute immune response secondary to STEC infection, the Stx stimulatory effect on different immune cells, and inflammatory stimulus secondary to endothelial damage all together converge to define a strong inflammatory status that worsens Stx toxicity and disease.
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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.