ArticleClinical and experimental immunology2006
Relevance of neutrophils in the murine model of haemolytic uraemic syndrome: mechanisms involved in Shiga toxin type 2-induced neutrophilia.
Article in Clinical and experimental immunology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.
- The emerging role of immunothrombosis in paediatric conditions.Pediatric research · 2019Pooled it
- Nutraceutical Potential of Djulis (Antioxidants (Basel, Switzerland) · 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
- Bruton's tyrosine kinase inhibition attenuates disease progression by reducing renal immune cell invasion in mice with hemolytic-uremic syndrome.Frontiers in immunology · 2023Article
- Verotoxin Receptor-Based Pathology and Therapies.Frontiers in cellular and infection microbiology · 2020Review
- Pathogenic role of inflammatory response during Shiga toxin-associated hemolytic uremic syndrome (HUS).Pediatric nephrology (Berlin, Germany) · 2018Review
- Modeling Hemolytic-Uremic Syndrome: In-Depth Characterization of Distinct Murine Models Reflecting Different Features of Human Disease.Frontiers in immunology · 2018Article
- Comparison of clinical and immunological findings in gnotobiotic piglets infected withGut pathogens · 2017Article
- Development of camelid single chain antibodies against Shiga toxin type 2 (Stx2) with therapeutic potential against Hemolytic Uremic Syndrome (HUS).Scientific reports · 2016Article
- Induction of Neutrophil Extracellular Traps in Shiga Toxin-Associated Hemolytic Uremic Syndrome.Journal of innate immunity · 2016Article
- Practical murine hematopathology: a comparative review and implications for research.Comparative medicine · 2015Review
- 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
- Hemolytic uremic syndrome: toxins, vessels, and inflammation.Frontiers in medicine · 2014Review
- Article
- Cytokine production is altered in monocytes from children with hemolytic uremic syndrome.Journal of clinical immunology · 2012Article
- Tolerance to lipopolysaccharide promotes an enhanced neutrophil extracellular traps formation leading to a more efficient bacterial clearance in mice.Clinical and experimental immunology · 2012Article
- Shiga toxin pathogenesis: kidney complications and renal failure.Current topics in microbiology and immunology · 2012Review
- Regulation of innate immune response to Candida albicans infections by αMβ2-Pra1p interaction.Infection and immunity · 2011Article
- Renal damage and death in weaned mice after oral infection with Shiga toxin 2-producing Escherichia coli strains.Clinical and experimental immunology · 2008Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It has been demonstrated that infections due to Shiga toxins (Stx) producing Escherichia coli are the main cause of the haemolytic uraemic syndrome (HUS). However, the contribution of the inflammatory response in the pathogenesis of the disease has also been well established. Neutrophils (PMN) represent a central component of inflammation during infections, and patients with high peripheral PMN counts at presentation have a poor prognosis. The mouse model of HUS, by intravenous injection of pure Stx type 2 (Stx2), reproduces human neutrophilia and allows the study of early events in the course of Stx2-induced pathophysiological mechanisms. The aim of this study was to address the contribution of PMN on Stx2 toxicity in a murine model of HUS, by evaluating the survival and renal damage in mice in which the granulocytic population was depleted. We found that the absence of PMN reduced Stx2-induced lethal effects and renal damage. We also investigated the mechanisms underlying Stx2-induced neutrophilia, studying the influence of Stx2 on myelopoyesis, on the emergence of cells from the bone marrow and on the in vivo migration into tissues. Stx2 administration led to an accelerated release of bone marrow cells, which egress at an earlier stage of maturation, together with an increase in the proliferation of myeloid progenitors. Moreover, Stx2-treated mice exhibited a lower migratory capacity to a local inflammatory site. In conclusion, PMN are essential in the pathogenesis of HUS and neutrophilia is not merely an epiphenomenon, but contributes to Stx2-damaging mechanism by potentiating Stx2 toxicity.
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