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Neutrophil, neutrophil extracellular traps and endothelial cell dysfunction in sepsis
Sepsis is a persistent systemic inflammatory condition involving multiple organ failures resulting from a dysregulated immune response to infection, and one of the hallmarks of sepsis is endothelial dysfunction. During its progression, neutrophils are the first line of innate immune defence against...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9832433/ https://www.ncbi.nlm.nih.gov/pubmed/36629024 http://dx.doi.org/10.1002/ctm2.1170 |
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author | Zhang, Hao Wang, Yanghanzhao Qu, Mengdi Li, Wenqian Wu, Dan Cata, Juan P. Miao, Changhong |
author_facet | Zhang, Hao Wang, Yanghanzhao Qu, Mengdi Li, Wenqian Wu, Dan Cata, Juan P. Miao, Changhong |
author_sort | Zhang, Hao |
collection | PubMed |
description | Sepsis is a persistent systemic inflammatory condition involving multiple organ failures resulting from a dysregulated immune response to infection, and one of the hallmarks of sepsis is endothelial dysfunction. During its progression, neutrophils are the first line of innate immune defence against infection. Aside from traditional mechanisms, such as phagocytosis or the release of inflammatory cytokines, reactive oxygen species and other antibacterial substances, activated neutrophils also release web‐like structures composed of tangled decondensed DNA, histone, myeloperoxidase and other granules called neutrophil extracellular traps (NETs), which can efficiently ensnare bacteria in the circulation. In contrast, excessive neutrophil activation and NET release may induce endothelial cells to shift toward a pro‐inflammatory and pro‐coagulant phenotype. Furthermore, neutrophils and NETs can degrade glycocalyx on the endothelial cell surface and increase endothelium permeability. Consequently, the endothelial barrier collapses, contributing to impaired microcirculatory blood flow, tissue hypoperfusion and life‐threatening organ failure in the late phase of sepsis. |
format | Online Article Text |
id | pubmed-9832433 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-98324332023-01-12 Neutrophil, neutrophil extracellular traps and endothelial cell dysfunction in sepsis Zhang, Hao Wang, Yanghanzhao Qu, Mengdi Li, Wenqian Wu, Dan Cata, Juan P. Miao, Changhong Clin Transl Med Reviews Sepsis is a persistent systemic inflammatory condition involving multiple organ failures resulting from a dysregulated immune response to infection, and one of the hallmarks of sepsis is endothelial dysfunction. During its progression, neutrophils are the first line of innate immune defence against infection. Aside from traditional mechanisms, such as phagocytosis or the release of inflammatory cytokines, reactive oxygen species and other antibacterial substances, activated neutrophils also release web‐like structures composed of tangled decondensed DNA, histone, myeloperoxidase and other granules called neutrophil extracellular traps (NETs), which can efficiently ensnare bacteria in the circulation. In contrast, excessive neutrophil activation and NET release may induce endothelial cells to shift toward a pro‐inflammatory and pro‐coagulant phenotype. Furthermore, neutrophils and NETs can degrade glycocalyx on the endothelial cell surface and increase endothelium permeability. Consequently, the endothelial barrier collapses, contributing to impaired microcirculatory blood flow, tissue hypoperfusion and life‐threatening organ failure in the late phase of sepsis. John Wiley and Sons Inc. 2023-01-11 /pmc/articles/PMC9832433/ /pubmed/36629024 http://dx.doi.org/10.1002/ctm2.1170 Text en © 2023 The Authors. Clinical and Translational Medicine published by John Wiley & Sons Australia, Ltd on behalf of Shanghai Institute of Clinical Bioinformatics. https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Reviews Zhang, Hao Wang, Yanghanzhao Qu, Mengdi Li, Wenqian Wu, Dan Cata, Juan P. Miao, Changhong Neutrophil, neutrophil extracellular traps and endothelial cell dysfunction in sepsis |
title | Neutrophil, neutrophil extracellular traps and endothelial cell dysfunction in sepsis |
title_full | Neutrophil, neutrophil extracellular traps and endothelial cell dysfunction in sepsis |
title_fullStr | Neutrophil, neutrophil extracellular traps and endothelial cell dysfunction in sepsis |
title_full_unstemmed | Neutrophil, neutrophil extracellular traps and endothelial cell dysfunction in sepsis |
title_short | Neutrophil, neutrophil extracellular traps and endothelial cell dysfunction in sepsis |
title_sort | neutrophil, neutrophil extracellular traps and endothelial cell dysfunction in sepsis |
topic | Reviews |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9832433/ https://www.ncbi.nlm.nih.gov/pubmed/36629024 http://dx.doi.org/10.1002/ctm2.1170 |
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