Education, Science, Technology, Innovation and Life
Open Access
Sign In
  1. Home
  2. Journals
  3. MEDS Clinical Medicine
  4. Vol 4, Issue 4, 2023

Research progress of NETs-mediated endothelial cell dysfunction in sepsis

Download as PDF

DOI: 10.23977/medsc.2023.040411 | Downloads: 13 | Views: 440

Author(s)

Meng Bi 1, Xiaohong Zhang 2

Affiliation(s)

1 School of Medical and Life Sciences, Chengdu University of Traditional Chinese Medicine, Chengdu, Sichuan, China
2 Department of Emergency Medicine, Sichuan Provincial People's Hospital, Chengdu, Sichuan, China

Corresponding Author

Xiaohong Zhang

ABSTRACT

Neutrophil extracellular traps (NETs), a network of DNA, histone, myeloperoxidase, and other particles released by activated neutrophils, can effectively capture circulating pathogens. Inappropriate neutrophil activation and NETs release in sepsis induce endothelial cells to turn to an inflammatory cascade, degrade the glycocalyx on the surface of endothelial cells, and increase endothelial cell permeability, leading to microcirculation disorders, tissue hypoperfusion and life-threatening organ dysfunction in the later stages of sepsis. This article summarizes the formation of NETs and elaborates the mechanism of nets-mediated endothelial cell dysfunction in sepsis, so as to provide a new direction for targeted therapy of sepsis.

KEYWORDS

Neutrophil extracellular traps, Endothelium cell, Sepsis

CITE THIS PAPER

Meng Bi, Xiaohong Zhang, Research progress of NETs-mediated endothelial cell dysfunction in sepsis. MEDS Clinical Medicine (2023) Vol. 4: 72-77. DOI: http://dx.doi.org/10.23977/medsc.2023.040411.

REFERENCES

[1] Evans L, Rhodes A, Alhazzani W, et al. Surviving sepsis campaign: international guidelines for management of sepsis and septic shock 2021 [J/OL]. Intensive Care Med, 2021: 1-67.
[2] Rosa BA, Ahmed M, Singh DK, et al. IFN signalling and neutrophil degranulation transcriptional signatures are induced during SARS‐CoV‐2 infection. Commun Biol. 2021; 4(1):290.
[3] Shen X, Cao K, Zhao Y, Du J. Targeting Neutrophils in Sepsis: From Mechanism to Translation. Front Pharmacol. 2021; 12:644270. Published 2021 Apr 12. 
[4] Joffre J, Hellman J, Ince C, Ait‐Oufella H. Endothelial responses in sepsis. Am J Respir Crit Care Med. 2020; 202(3): 361‐370. 
[5] Brinkmann V, Reichard U, Goosmann C, et al. Neutrophil extracellular traps kill bacteria. Science. 2004; 303(5663): 1532‐1535. 
[6] Klopf J, Brostjan C, Eilenberg W, Neumayer C. Neutrophil Extracellular Traps and Their Implications in Cardiovascular and Inflammatory Disease. Int J Mol Sci. 2021; 22(2):559. Published 2021 Jan 8.
[7] Nagaoka I, Tamura H, Reich J. Therapeutic potential of cathelicidin peptide LL‐37, an antimicrobial agent, in a murine sepsis model. Int J Mol Sci. 2020; 21(17):E5973. 
[8] Li Y, Chen Y, Yang T, et al. Targeting circulating high mobility group box-1 and histones by extracorporeal blood purification as an immunomodulation strategy against critical illnesses. Crit Care. 2023; 27(1):77. Published 2023 Feb 28. 
[9] Fernandez S, Brown‐Chestnut AB, Dove M, et al. Distinctive biomarker features in the endotheliopathy of COPD and septic syndromes. Shock Augusta Ga. 2022; 57(1):95‐105. 
[10] Iba T, Levi M, Levy JH. Sepsis‐induced coagulopathy and disseminated intravascular coagulation. Semin Thromb Hemost. 2020; 46(01):089‐095.
[11] Chen Z, Zhang H, Qu M, et al. Review: the emerging role of neutrophil extracellular traps in sepsis and sepsis‐associated thrombosis. Front Cell Infect Microbiol. 2021; 11:653228. 
[12] Schönrich G, Raftery MJ, Samstag Y. Devilishly radical NETwork in COVID-19: Oxidative stress, neutrophil extracellular traps (NETs), and T cell suppression. Adv Biol Regul. 2020; 77:100741.
[13] Zhang H, Wang Y, Qu M, et al. Neutrophil, neutrophil extracellular traps and endothelial cell dysfunction in sepsis. Clin Transl Med. 2023; 13(1):e1170.
[14] Gao F, Sun H, Li X, He P. Leveraging avidin-biotin interaction to quantify permeability property of microvessels-on-a-chip networks. Am J Physiol Heart Circ Physiol. 2022; 322(1):H71-H86. 
[15] Vahldieck C, Cianflone E, Fels B, et al. Endothelial Glycocalyx and Cardiomyocyte Damage Is Prevented by Recombinant Syndecan-1 in Acute Myocardial Infarction. Am J Pathol. 2023; 193(4):474-492.
[16] Parthasarathy U, Kuang Y, Thakur G, et al. Distinct subsets of neutrophils crosstalk with cytokines and metabolites in patients with sepsis. iScience. 2023; 26(2):105948. Published 2023 Jan 7.
[17] Wautier JL, Wautier MP. Vascular permeability in diseases. Int J Mol Sci. 2022; 23(7):3645.
[18] Tetz G, Tetz V. Introducing the extrabiome and its classification: a new view on extracellular nucleic acids. Future Microbiol. 2023; 18:181-184.
[19] Ciesielska S, Bil P, Gajda K, Poterala-Hejmo A, Hudy D, Rzeszowska-Wolny J. Cell type-specific differences in redox regulation and proliferation after low UVA doses. PLOS One. 2019; 14(1):e0205215. Published 2019 Jan 25.
[20] Sumagin R, Kuebel JM, Sarelius IH. Leukocyte rolling and adhesion both contribute to regulation of microvascular permeability to albumin via ligation of ICAM‐1. Am J Physiol Cell Physiol. 2011; 301(4):C804‐813.
[21] Lund M, Macwan AS, Tunströmer K, Lindahl TL, Boknäs N. Effects of Heparin and Bivalirudin on Thrombin-Induced Platelet Activation: Differential Modulation of PAR Signaling Drives Divergent Prothrombotic Responses. Front Cardiovasc Med. 2021; 8:717835. Published 2021 Sep 29.
[22] Maltabe V, Kouklis P. Vascular Endothelial (VE)-cadherin-mediated adherens junctions involvement in cardiovascular progenitor cell specification. Int J Dev Biol. 2022; 66(1-2-3):77-83.
[23] Wu B, Xu MM, Fan C, et al. STING inhibitor ameliorates LPS-induced ALI by preventing vascular endothelial cells-mediated immune cells chemotaxis and adhesion. Acta Pharmacol Sin. 2022; 43(8):2055-2066.
[24] Martinod K, Fuchs TA, Zitomersky NL, et al. PAD4‐deficiency does not affect bacteremia in polymicrobial sepsis and ameliorates endotoxemic shock. Blood. 2015; 125(12):1948‐1956. 
[25] Dou Q, Grant AK, Callahan C, et al. PFKFB3-mediated Pro-glycolytic Shift in Hepatocellular Carcinoma Proliferation. Cell Mol Gastroenterol Hepatol. 2023; 15(1):61-75. 
[26] Cui C, Chakraborty K, Tang XA, et al. Neutrophil elastase selectively kills cancer cells and attenuates tumorigenesis. Cell. 2021; 184(12):3163-3177.e21.
[27] Thiam HR, Wong SL, Qiu R, et al. NETosis proceeds by cytoskeleton and endomembrane disassembly and PAD4‐mediated chromatin decondensation and nuclear envelope rupture. Proc Natl Acad Sci U S A. 2020; 117(13): 7326‐7337. 
[28] Ziogas A, Sajib MS, Lim JH, et al. Glycolysis is integral to histamine-induced endothelial hyperpermeability. FASEB J. 2021; 35(3):e21425.

Subscription
E-Mail Alert
Most popular papers
Call for Special Issue
Publication Ethics & OA Statement
Plagiarism Policy
Contact Us
Downloads: 4674
Visits: 203939

Sponsors, Associates, and Links

All published work is licensed under a Creative Commons Attribution 4.0 International License.

Copyright © 2016 - 2031 Clausius Scientific Press Inc. All Rights Reserved.