Innate Immune Cells and Hypertension: Neutrophils and Neutrophil Extracellular Traps (NETs).
COVID-19
blood pressure
gut microbiota
immune system
myeloid-derived immune cells
neutrophils
oxidative stress
Journal
Comprehensive Physiology
ISSN: 2040-4603
Titre abrégé: Compr Physiol
Pays: United States
ID NLM: 101574442
Informations de publication
Date de publication:
12 02 2021
12 02 2021
Historique:
entrez:
12
2
2021
pubmed:
13
2
2021
medline:
20
2
2021
Statut:
epublish
Résumé
Uncontrolled immune system activation amplifies end-organ injury in hypertension. Nonetheless, the exact mechanisms initiating this exacerbated inflammatory response, thereby contributing to further increases in blood pressure (BP), are still being revealed. While participation of lymphoid-derived immune cells has been well described in the hypertension literature, the mechanisms by which myeloid-derived innate immune cells contribute to T cell activation, and subsequent BP elevation, remains an active area of investigation. In this article, we critically analyze the literature to understand how monocytes, macrophages, dendritic cells, and polymorphonuclear leukocytes, including mast cells, eosinophils, basophils, and neutrophils, contribute to hypertension and hypertension-associated end-organ injury. The most abundant leukocytes, neutrophils, are indisputably increased in hypertension. However, it is unknown how (and why) they switch from critical first responders of the innate immune system, and homeostatic regulators of BP, to tissue-damaging, pro-hypertensive mediators. We propose that myeloperoxidase-derived pro-oxidants, neutrophil elastase, neutrophil extracellular traps (NETs), and interactions with other innate and adaptive immune cells are novel mechanisms that could contribute to the inflammatory cascade in hypertension. We further posit that the gut microbiota serves as a set point for neutropoiesis and their function. Finally, given that hypertension appears to be a key risk factor for morbidity and mortality in COVID-19 patients, we put forth evidence that neutrophils and NETs cause cardiovascular injury post-coronavirus infection, and thus may be proposed as an intriguing therapeutic target for high-risk individuals. © 2021 American Physiological Society. Compr Physiol 11:1575-1589, 2021.
Identifiants
pubmed: 33577121
doi: 10.1002/cphy.c200020
pmc: PMC9721119
mid: NIHMS1850959
doi:
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
1575-1589Subventions
Organisme : NCI NIH HHS
ID : R01 CA219144
Pays : United States
Organisme : NHLBI NIH HHS
ID : K99 HL151889
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL149762
Pays : United States
Organisme : NIGMS NIH HHS
ID : K99 GM118885
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL143082
Pays : United States
Organisme : NHLBI NIH HHS
ID : R00 HL151889
Pays : United States
Organisme : NIGMS NIH HHS
ID : R00 GM118885
Pays : United States
Informations de copyright
Copyright © 2021 American Physiological Society. All rights reserved.
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