ArticlePLoS pathogens2015
A novel mechanism of bacterial toxin transfer within host blood cell-derived microvesicles.
Article in PLoS pathogens, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.
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Who cites it
71 citing papers in PubMed.
- TLR4: A Potential Therapeutic Target in the Experimental Pathogenesis of Hemolytic-Uremic Syndrome.International journal of molecular sciences · 2026Article
- Shiga toxin delivery in extracellular vesicles induces high mortality and severe kidney injury in a Gb3-dependent manner.PLoS pathogens · 2026Article
- Molecular determinants of STEC-HUS: from complement activation to microvascular thrombosis.Frontiers in immunology · 2026Article
- Cellular signaling pathway of Shiga toxin-induced ATP release.Frontiers in cellular and infection microbiology · 2026Article
- An antibiotic derivative as a new potential tool in the prevention of hemolytic uremic syndrome.iScience · 2025Article
- Neurological Manifestations of Hemolytic Uremic Syndrome: A Comprehensive Review.Brain sciences · 2025Review
- Monocytes serve as Shiga toxin carriers during the development of hemolytic uremic syndrome.Cellular & molecular biology letters · 2025Article
- EnterohemorrhagicFrontiers in cellular and infection microbiology · 2025Article
- Article
- Strategies for non-viral vectors targeting organs beyond the liver.Nature nanotechnology · 2024Review
- Red blood cell-derived arginase release in hemolytic uremic syndrome.Journal of translational medicine · 2024Article
- The Role of the Complement System in the Pathogenesis of Infectious Forms of Hemolytic Uremic Syndrome.Biomolecules · 2023Review
- Article
- The role of pneumococcal extracellular vesicles on the pathophysiology of the kidney disease hemolytic uremic syndrome.mSphere · 2023Article
- The Fatal Role of Enterohaemorrhagic Escherichia coli Shiga Toxin-associated Extracellular Vesicles in Host Cells.Journal of microbiology (Seoul, Korea) · 2023Review
- Extracellular Vesicle MicroRNA in the Kidney.Comprehensive Physiology · 2023Article
- The biodistribution of placental and fetal extracellular vesicles during pregnancy following placentation.Clinical science (London, England : 1979) · 2023Article
- Shiga Toxin (Stx) Type 1a and Stx2a Translocate through a Three-Layer Intestinal Model.Toxins · 2023Article
- ABToxins · 2022Review
- Roles of MicroRNA-21 in Skin Wound Healing: A Comprehensive Review.Frontiers in pharmacology · 2022Review
11 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Shiga toxin (Stx) is the main virulence factor of enterohemorrhagic Escherichia coli, which are non-invasive strains that can lead to hemolytic uremic syndrome (HUS), associated with renal failure and death. Although bacteremia does not occur, bacterial virulence factors gain access to the circulation and are thereafter presumed to cause target organ damage. Stx was previously shown to circulate bound to blood cells but the mechanism by which it would potentially transfer to target organ cells has not been elucidated. Here we show that blood cell-derived microvesicles, shed during HUS, contain Stx and are found within patient renal cortical cells. The finding was reproduced in mice infected with Stx-producing Escherichia coli exhibiting Stx-containing blood cell-derived microvesicles in the circulation that reached the kidney where they were transferred into glomerular and peritubular capillary endothelial cells and further through their basement membranes followed by podocytes and tubular epithelial cells, respectively. In vitro studies demonstrated that blood cell-derived microvesicles containing Stx undergo endocytosis in glomerular endothelial cells leading to cell death secondary to inhibited protein synthesis. This study demonstrates a novel virulence mechanism whereby bacterial toxin is transferred within host blood cell-derived microvesicles in which it may evade the host immune system.
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