ArticlePediatric nephrology (Berlin, Germany)2005
Impaired neutrophils in children with the typical form of hemolytic uremic syndrome.
Article in Pediatric nephrology (Berlin, Germany), 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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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
14 citing papers in PubMed, 37 citations in OpenAlex.
- Factors affecting dialysis duration in children with Shiga toxin-producing Escherichia coli-associated hemolytic uremic syndrome.Pediatric nephrology (Berlin, Germany) · 2023Article
- Shiga Toxin 2a Induces NETosis via NOX-Dependent Pathway.Biomedicines · 2021Article
- Pathogenic role of inflammatory response during Shiga toxin-associated hemolytic uremic syndrome (HUS).Pediatric nephrology (Berlin, Germany) · 2018Review
- Induction of Neutrophil Extracellular Traps in Shiga Toxin-Associated Hemolytic Uremic Syndrome.Journal of innate immunity · 2016Article
- Natural killer T (NKT) cells accelerate Shiga toxin type 2 (Stx2) pathology in mice.Frontiers in microbiology · 2015Article
- Retinoid levels influence enterohemorrhagic Escherichia coli infection and Shiga toxin 2 susceptibility in mice.Infection and immunity · 2014Article
- The oxidative stress induced in vivo by Shiga toxin-2 contributes to the pathogenicity of haemolytic uraemic syndrome.Clinical and experimental immunology · 2013Article
- Toll-like receptor 4 expression on circulating leucocytes in hemolytic uremic syndrome.Pediatric nephrology (Berlin, Germany) · 2012Article
- The interactions of human neutrophils with shiga toxins and related plant toxins: danger or safety?Toxins · 2012Review
- Shiga toxin pathogenesis: kidney complications and renal failure.Current topics in microbiology and immunology · 2012Review
- Change in conformation with reduction of alpha-helix content causes loss of neutrophil binding activity in fully cytotoxic Shiga toxin 1.The Journal of biological chemistry · 2011Article
- Shiga toxin-associated hemolytic uremic syndrome: pathophysiology of endothelial dysfunction.Pediatric nephrology (Berlin, Germany) · 2010Review
- Shiga toxin 1-induced inflammatory response in lipopolysaccharide-sensitized astrocytes is mediated by endogenous tumor necrosis factor alpha.Infection and immunity · 2010Article
- Comparative analysis of the abilities of Shiga toxins 1 and 2 to bind to and influence neutrophil apoptosis.Infection and immunity · 2007Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Experimental and clinical evidence suggest that activated neutrophils (PMN) could contribute to endothelial damage in Hemolytic Uremic Syndrome (D+HUS). Additionally, while PMN-activating cytokines and PMN-derived products have been found in D+HUS sera, we have demonstrated phenotypic alterations in D+HUS PMN compatible with a deactivation state. Here, we investigated whether D+HUS PMN were actually hyporesponsive, and explored some of the mechanisms probably involved in their derangement. Twenty-two D+HUS children were bled in the acute period, and blood samples from healthy, acute uremic and neutrophilic children were obtained as controls. We evaluated degranulation markers in response to cytokines, intracellular granule content, and reactive oxygen species (ROS) generation in circulating D+HUS and control PMN. The influence of D+HUS-derived plasma and the direct effects of Stx in vitro were evaluated on healthy donors' PMN. We found that D+HUS PMN presented reduced degranulatory capacity in response to cytokines and intracellular granule content, and decreased ROS generation. D+HUS plasma or Stx did not affect the phenotype and function of healthy donors' PMN. These results suggest that upon hospitalization D+HUS PMN are functionally impaired and show features of previous degranulation, indicating a preceding process of activation with release of ROS and proteases involved in endothelial damage.
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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.