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Endothelial dysfunction and immunothrombosis in sepsis

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Endothelial dysfunction and immunothrombosis in sepsis. / Maneta, Eleni; Aivalioti, Evmorfia; Tual-Chalot, Simon et al.
In: Frontiers in Immunology, Vol. 14, 1144229, 04.04.2023.

Research output: Contribution to Journal/MagazineReview articlepeer-review

Harvard

Maneta, E, Aivalioti, E, Tual-Chalot, S, Emini Veseli, B, Gatsiou, A, Stamatelopoulos, K & Stellos, K 2023, 'Endothelial dysfunction and immunothrombosis in sepsis', Frontiers in Immunology, vol. 14, 1144229. https://doi.org/10.3389/fimmu.2023.1144229

APA

Maneta, E., Aivalioti, E., Tual-Chalot, S., Emini Veseli, B., Gatsiou, A., Stamatelopoulos, K., & Stellos, K. (2023). Endothelial dysfunction and immunothrombosis in sepsis. Frontiers in Immunology, 14, Article 1144229. https://doi.org/10.3389/fimmu.2023.1144229

Vancouver

Maneta E, Aivalioti E, Tual-Chalot S, Emini Veseli B, Gatsiou A, Stamatelopoulos K et al. Endothelial dysfunction and immunothrombosis in sepsis. Frontiers in Immunology. 2023 Apr 4;14:1144229. doi: 10.3389/fimmu.2023.1144229

Author

Maneta, Eleni ; Aivalioti, Evmorfia ; Tual-Chalot, Simon et al. / Endothelial dysfunction and immunothrombosis in sepsis. In: Frontiers in Immunology. 2023 ; Vol. 14.

Bibtex

@article{93d241d0c20340bc8ecb1088a66e801d,
title = "Endothelial dysfunction and immunothrombosis in sepsis",
abstract = "Sepsis is a life-threatening clinical syndrome characterized by multiorgan dysfunction caused by a dysregulated or over-reactive host response to infection. During sepsis, the coagulation cascade is triggered by activated cells of the innate immune system, such as neutrophils and monocytes, resulting in clot formation mainly in the microcirculation, a process known as immunothrombosis. Although this process aims to protect the host through inhibition of the pathogen's dissemination and survival, endothelial dysfunction and microthrombotic complications can rapidly lead to multiple organ dysfunction. The development of treatments targeting endothelial innate immune responses and immunothrombosis could be of great significance for reducing morbidity and mortality in patients with sepsis. Medications modifying cell-specific immune responses or inhibiting platelet-endothelial interaction or platelet activation have been proposed. Herein, we discuss the underlying mechanisms of organ-specific endothelial dysfunction and immunothrombosis in sepsis and its complications, while highlighting the recent advances in the development of new therapeutic approaches aiming at improving the short- or long-term prognosis in sepsis.",
keywords = "Humans, Thromboinflammation, Vascular Diseases, Sepsis, Neutrophils, Thrombosis",
author = "Eleni Maneta and Evmorfia Aivalioti and Simon Tual-Chalot and {Emini Veseli}, Besa and Aikaterini Gatsiou and Kimon Stamatelopoulos and Konstantinos Stellos",
note = "Copyright {\textcopyright} 2023 Maneta, Aivalioti, Tual-Chalot, Emini Veseli, Gatsiou, Stamatelopoulos and Stellos.",
year = "2023",
month = apr,
day = "4",
doi = "10.3389/fimmu.2023.1144229",
language = "English",
volume = "14",
journal = "Frontiers in Immunology",
issn = "1664-3224",
publisher = "Frontiers Media S.A.",

}

RIS

TY - JOUR

T1 - Endothelial dysfunction and immunothrombosis in sepsis

AU - Maneta, Eleni

AU - Aivalioti, Evmorfia

AU - Tual-Chalot, Simon

AU - Emini Veseli, Besa

AU - Gatsiou, Aikaterini

AU - Stamatelopoulos, Kimon

AU - Stellos, Konstantinos

N1 - Copyright © 2023 Maneta, Aivalioti, Tual-Chalot, Emini Veseli, Gatsiou, Stamatelopoulos and Stellos.

PY - 2023/4/4

Y1 - 2023/4/4

N2 - Sepsis is a life-threatening clinical syndrome characterized by multiorgan dysfunction caused by a dysregulated or over-reactive host response to infection. During sepsis, the coagulation cascade is triggered by activated cells of the innate immune system, such as neutrophils and monocytes, resulting in clot formation mainly in the microcirculation, a process known as immunothrombosis. Although this process aims to protect the host through inhibition of the pathogen's dissemination and survival, endothelial dysfunction and microthrombotic complications can rapidly lead to multiple organ dysfunction. The development of treatments targeting endothelial innate immune responses and immunothrombosis could be of great significance for reducing morbidity and mortality in patients with sepsis. Medications modifying cell-specific immune responses or inhibiting platelet-endothelial interaction or platelet activation have been proposed. Herein, we discuss the underlying mechanisms of organ-specific endothelial dysfunction and immunothrombosis in sepsis and its complications, while highlighting the recent advances in the development of new therapeutic approaches aiming at improving the short- or long-term prognosis in sepsis.

AB - Sepsis is a life-threatening clinical syndrome characterized by multiorgan dysfunction caused by a dysregulated or over-reactive host response to infection. During sepsis, the coagulation cascade is triggered by activated cells of the innate immune system, such as neutrophils and monocytes, resulting in clot formation mainly in the microcirculation, a process known as immunothrombosis. Although this process aims to protect the host through inhibition of the pathogen's dissemination and survival, endothelial dysfunction and microthrombotic complications can rapidly lead to multiple organ dysfunction. The development of treatments targeting endothelial innate immune responses and immunothrombosis could be of great significance for reducing morbidity and mortality in patients with sepsis. Medications modifying cell-specific immune responses or inhibiting platelet-endothelial interaction or platelet activation have been proposed. Herein, we discuss the underlying mechanisms of organ-specific endothelial dysfunction and immunothrombosis in sepsis and its complications, while highlighting the recent advances in the development of new therapeutic approaches aiming at improving the short- or long-term prognosis in sepsis.

KW - Humans

KW - Thromboinflammation

KW - Vascular Diseases

KW - Sepsis

KW - Neutrophils

KW - Thrombosis

U2 - 10.3389/fimmu.2023.1144229

DO - 10.3389/fimmu.2023.1144229

M3 - Review article

C2 - 37081895

VL - 14

JO - Frontiers in Immunology

JF - Frontiers in Immunology

SN - 1664-3224

M1 - 1144229

ER -