Host-derived microvesicles carrying bacterial pore-forming toxins deliver signals to macrophages: a novel mechanism of shaping immune responses

Research output: Contribution to journalArticlepeer-review

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Host-derived microvesicles carrying bacterial pore-forming toxins deliver signals to macrophages : a novel mechanism of shaping immune responses. / Köffel, René; Wolfmeier, Heidi; Larpin, Yu; Besançon, Hervé; Schoenauer, Roman; Babiychuk, Viktoria S; Drücker, Patrick; Pabst, Thomas; Mitchell, Timothy J; Babiychuk, Eduard B; Draeger, Annette.

In: Frontiers in immunology, Vol. 9, 1688, 27.07.2018.

Research output: Contribution to journalArticlepeer-review

Harvard

Köffel, R, Wolfmeier, H, Larpin, Y, Besançon, H, Schoenauer, R, Babiychuk, VS, Drücker, P, Pabst, T, Mitchell, TJ, Babiychuk, EB & Draeger, A 2018, 'Host-derived microvesicles carrying bacterial pore-forming toxins deliver signals to macrophages: a novel mechanism of shaping immune responses', Frontiers in immunology, vol. 9, 1688. https://doi.org/10.3389/fimmu.2018.01688

APA

Köffel, R., Wolfmeier, H., Larpin, Y., Besançon, H., Schoenauer, R., Babiychuk, V. S., Drücker, P., Pabst, T., Mitchell, T. J., Babiychuk, E. B., & Draeger, A. (2018). Host-derived microvesicles carrying bacterial pore-forming toxins deliver signals to macrophages: a novel mechanism of shaping immune responses. Frontiers in immunology, 9, [1688]. https://doi.org/10.3389/fimmu.2018.01688

Vancouver

Author

Köffel, René ; Wolfmeier, Heidi ; Larpin, Yu ; Besançon, Hervé ; Schoenauer, Roman ; Babiychuk, Viktoria S ; Drücker, Patrick ; Pabst, Thomas ; Mitchell, Timothy J ; Babiychuk, Eduard B ; Draeger, Annette. / Host-derived microvesicles carrying bacterial pore-forming toxins deliver signals to macrophages : a novel mechanism of shaping immune responses. In: Frontiers in immunology. 2018 ; Vol. 9.

Bibtex

@article{8d566fe8513f402f8b408648a4628a5a,
title = "Host-derived microvesicles carrying bacterial pore-forming toxins deliver signals to macrophages: a novel mechanism of shaping immune responses",
abstract = "Bacterial infectious diseases are a leading cause of death. Pore-forming toxins (PFTs) are important virulence factors of Gram-positive pathogens, which disrupt the plasma membrane of host cells and can lead to cell death. Yet, host defense and cell membrane repair mechanisms have been identified: i.e., PFTs can be eliminated from membranes as microvesicles, thus limiting the extent of cell damage. Released into an inflammatory environment, these host-derived PFTs-carrying microvesicles encounter innate immune cells as first-line defenders. This study investigated the impact of microvesicle- or liposome-sequestered PFTs on human macrophage polarization in vitro. We show that microvesicle-sequestered PFTs are phagocytosed by macrophages and induce their polarization into a novel CD14+MHCIIlowCD86low phenotype. Macrophages polarized in this way exhibit an enhanced response to Gram-positive bacterial ligands and a blunted response to Gram-negative ligands. Liposomes, which were recently shown to sequester PFTs and so protect mice from lethal bacterial infections, show the same effect on macrophage polarization in analogy to host-derived microvesicles. This novel type of polarized macrophage exhibits an enhanced response to Gram-positive bacterial ligands. The specific recognition of their cargo might be of advantage in the efficiency of targeted bacterial clearance.",
keywords = "macrophage polarization, microvesicles, liposomes, bacterial pore-forming toxins, host-defense",
author = "Ren{\'e} K{\"o}ffel and Heidi Wolfmeier and Yu Larpin and Herv{\'e} Besan{\c c}on and Roman Schoenauer and Babiychuk, {Viktoria S} and Patrick Dr{\"u}cker and Thomas Pabst and Mitchell, {Timothy J} and Babiychuk, {Eduard B} and Annette Draeger",
year = "2018",
month = jul,
day = "27",
doi = "10.3389/fimmu.2018.01688",
language = "English",
volume = "9",
journal = "Frontiers in immunology",
issn = "1664-3224",
publisher = "Frontiers",

}

RIS

TY - JOUR

T1 - Host-derived microvesicles carrying bacterial pore-forming toxins deliver signals to macrophages

T2 - a novel mechanism of shaping immune responses

AU - Köffel, René

AU - Wolfmeier, Heidi

AU - Larpin, Yu

AU - Besançon, Hervé

AU - Schoenauer, Roman

AU - Babiychuk, Viktoria S

AU - Drücker, Patrick

AU - Pabst, Thomas

AU - Mitchell, Timothy J

AU - Babiychuk, Eduard B

AU - Draeger, Annette

PY - 2018/7/27

Y1 - 2018/7/27

N2 - Bacterial infectious diseases are a leading cause of death. Pore-forming toxins (PFTs) are important virulence factors of Gram-positive pathogens, which disrupt the plasma membrane of host cells and can lead to cell death. Yet, host defense and cell membrane repair mechanisms have been identified: i.e., PFTs can be eliminated from membranes as microvesicles, thus limiting the extent of cell damage. Released into an inflammatory environment, these host-derived PFTs-carrying microvesicles encounter innate immune cells as first-line defenders. This study investigated the impact of microvesicle- or liposome-sequestered PFTs on human macrophage polarization in vitro. We show that microvesicle-sequestered PFTs are phagocytosed by macrophages and induce their polarization into a novel CD14+MHCIIlowCD86low phenotype. Macrophages polarized in this way exhibit an enhanced response to Gram-positive bacterial ligands and a blunted response to Gram-negative ligands. Liposomes, which were recently shown to sequester PFTs and so protect mice from lethal bacterial infections, show the same effect on macrophage polarization in analogy to host-derived microvesicles. This novel type of polarized macrophage exhibits an enhanced response to Gram-positive bacterial ligands. The specific recognition of their cargo might be of advantage in the efficiency of targeted bacterial clearance.

AB - Bacterial infectious diseases are a leading cause of death. Pore-forming toxins (PFTs) are important virulence factors of Gram-positive pathogens, which disrupt the plasma membrane of host cells and can lead to cell death. Yet, host defense and cell membrane repair mechanisms have been identified: i.e., PFTs can be eliminated from membranes as microvesicles, thus limiting the extent of cell damage. Released into an inflammatory environment, these host-derived PFTs-carrying microvesicles encounter innate immune cells as first-line defenders. This study investigated the impact of microvesicle- or liposome-sequestered PFTs on human macrophage polarization in vitro. We show that microvesicle-sequestered PFTs are phagocytosed by macrophages and induce their polarization into a novel CD14+MHCIIlowCD86low phenotype. Macrophages polarized in this way exhibit an enhanced response to Gram-positive bacterial ligands and a blunted response to Gram-negative ligands. Liposomes, which were recently shown to sequester PFTs and so protect mice from lethal bacterial infections, show the same effect on macrophage polarization in analogy to host-derived microvesicles. This novel type of polarized macrophage exhibits an enhanced response to Gram-positive bacterial ligands. The specific recognition of their cargo might be of advantage in the efficiency of targeted bacterial clearance.

KW - macrophage polarization

KW - microvesicles

KW - liposomes

KW - bacterial pore-forming toxins

KW - host-defense

U2 - 10.3389/fimmu.2018.01688

DO - 10.3389/fimmu.2018.01688

M3 - Article

C2 - 30100903

VL - 9

JO - Frontiers in immunology

JF - Frontiers in immunology

SN - 1664-3224

M1 - 1688

ER -