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A novel mechanism of bacterial toxin transfer within host blood cell-derived microvesicles

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A novel mechanism of bacterial toxin transfer within host blood cell-derived microvesicles. / Ståhl, Anne-lie; Arvidsson, Ida; Johansson, Karl E; Chromek, Milan; Rebetz, Johan; Loos, Sebastian; Kristoffersson, Ann-Charlotte; Békássy, Zivile D; Mörgelin, Matthias; Karpman, Diana.

in: PLOS PATHOG, Jahrgang 11, Nr. 2, 02.2015, S. e1004619.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Ståhl, A, Arvidsson, I, Johansson, KE, Chromek, M, Rebetz, J, Loos, S, Kristoffersson, A-C, Békássy, ZD, Mörgelin, M & Karpman, D 2015, 'A novel mechanism of bacterial toxin transfer within host blood cell-derived microvesicles', PLOS PATHOG, Jg. 11, Nr. 2, S. e1004619. https://doi.org/10.1371/journal.ppat.1004619

APA

Ståhl, A., Arvidsson, I., Johansson, K. E., Chromek, M., Rebetz, J., Loos, S., Kristoffersson, A-C., Békássy, Z. D., Mörgelin, M., & Karpman, D. (2015). A novel mechanism of bacterial toxin transfer within host blood cell-derived microvesicles. PLOS PATHOG, 11(2), e1004619. https://doi.org/10.1371/journal.ppat.1004619

Vancouver

Ståhl A, Arvidsson I, Johansson KE, Chromek M, Rebetz J, Loos S et al. A novel mechanism of bacterial toxin transfer within host blood cell-derived microvesicles. PLOS PATHOG. 2015 Feb;11(2):e1004619. https://doi.org/10.1371/journal.ppat.1004619

Bibtex

@article{bd11f1bdc710468ca8c9089be9e47580,
title = "A novel mechanism of bacterial toxin transfer within host blood cell-derived microvesicles",
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.",
keywords = "Adolescent, Adult, Animals, Bacterial Toxins, Blood Cells, Cell-Derived Microparticles, Cells, Cultured, Child, Child, Preschool, Enterohemorrhagic Escherichia coli, Escherichia coli Infections, Female, Host-Pathogen Interactions, Humans, Infant, Male, Mice, Mice, Inbred BALB C, Protein Transport, Journal Article, Research Support, Non-U.S. Gov't",
author = "Anne-lie St{\aa}hl and Ida Arvidsson and Johansson, {Karl E} and Milan Chromek and Johan Rebetz and Sebastian Loos and Ann-Charlotte Kristoffersson and B{\'e}k{\'a}ssy, {Zivile D} and Matthias M{\"o}rgelin and Diana Karpman",
year = "2015",
month = feb,
doi = "10.1371/journal.ppat.1004619",
language = "English",
volume = "11",
pages = "e1004619",
journal = "PLOS PATHOG",
issn = "1553-7366",
publisher = "Public Library of Science",
number = "2",

}

RIS

TY - JOUR

T1 - A novel mechanism of bacterial toxin transfer within host blood cell-derived microvesicles

AU - Ståhl, Anne-lie

AU - Arvidsson, Ida

AU - Johansson, Karl E

AU - Chromek, Milan

AU - Rebetz, Johan

AU - Loos, Sebastian

AU - Kristoffersson, Ann-Charlotte

AU - Békássy, Zivile D

AU - Mörgelin, Matthias

AU - Karpman, Diana

PY - 2015/2

Y1 - 2015/2

N2 - 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.

AB - 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.

KW - Adolescent

KW - Adult

KW - Animals

KW - Bacterial Toxins

KW - Blood Cells

KW - Cell-Derived Microparticles

KW - Cells, Cultured

KW - Child

KW - Child, Preschool

KW - Enterohemorrhagic Escherichia coli

KW - Escherichia coli Infections

KW - Female

KW - Host-Pathogen Interactions

KW - Humans

KW - Infant

KW - Male

KW - Mice

KW - Mice, Inbred BALB C

KW - Protein Transport

KW - Journal Article

KW - Research Support, Non-U.S. Gov't

U2 - 10.1371/journal.ppat.1004619

DO - 10.1371/journal.ppat.1004619

M3 - SCORING: Journal article

C2 - 25719452

VL - 11

SP - e1004619

JO - PLOS PATHOG

JF - PLOS PATHOG

SN - 1553-7366

IS - 2

ER -