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Periodontitis-Derived Dark-NETs in Severe Covid-19
by
Krunić, Jelena
, Herrmann, Martin
, Minnich, Bernd
, Vitkov, Ljubomir
, Knopf, Jasmin
, Schauer, Christine
, Schoen, Janina
, Hannig, Matthias
in
Cardiovascular diseases
/ Chemokines
/ Comorbidity
/ COVID-19
/ Cytokines
/ Deoxyribonuclease
/ Diabetes mellitus
/ dysregulated immunity
/ Endotoxemia
/ Endotoxemia - metabolism
/ Extracellular Traps
/ Gum disease
/ Humans
/ Immunity (Disease)
/ Immunology
/ Inflammation
/ inhibition of NET formation
/ Innate immunity
/ Leukocytes (neutrophilic)
/ Lipopolysaccharides
/ Lipopolysaccharides - metabolism
/ Lupus
/ NET hyper-responsiveness
/ NET-induced damage
/ neutrophil hyper-responsiveness
/ Neutrophils
/ Pathogens
/ Periodontitis
/ Periodontitis - pathology
/ Proteins
/ SARS-CoV-2
/ Severe acute respiratory syndrome coronavirus 2
/ Spike Glycoprotein, Coronavirus
/ Spike protein
/ trained immunity
2022
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Periodontitis-Derived Dark-NETs in Severe Covid-19
by
Krunić, Jelena
, Herrmann, Martin
, Minnich, Bernd
, Vitkov, Ljubomir
, Knopf, Jasmin
, Schauer, Christine
, Schoen, Janina
, Hannig, Matthias
in
Cardiovascular diseases
/ Chemokines
/ Comorbidity
/ COVID-19
/ Cytokines
/ Deoxyribonuclease
/ Diabetes mellitus
/ dysregulated immunity
/ Endotoxemia
/ Endotoxemia - metabolism
/ Extracellular Traps
/ Gum disease
/ Humans
/ Immunity (Disease)
/ Immunology
/ Inflammation
/ inhibition of NET formation
/ Innate immunity
/ Leukocytes (neutrophilic)
/ Lipopolysaccharides
/ Lipopolysaccharides - metabolism
/ Lupus
/ NET hyper-responsiveness
/ NET-induced damage
/ neutrophil hyper-responsiveness
/ Neutrophils
/ Pathogens
/ Periodontitis
/ Periodontitis - pathology
/ Proteins
/ SARS-CoV-2
/ Severe acute respiratory syndrome coronavirus 2
/ Spike Glycoprotein, Coronavirus
/ Spike protein
/ trained immunity
2022
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Periodontitis-Derived Dark-NETs in Severe Covid-19
by
Krunić, Jelena
, Herrmann, Martin
, Minnich, Bernd
, Vitkov, Ljubomir
, Knopf, Jasmin
, Schauer, Christine
, Schoen, Janina
, Hannig, Matthias
in
Cardiovascular diseases
/ Chemokines
/ Comorbidity
/ COVID-19
/ Cytokines
/ Deoxyribonuclease
/ Diabetes mellitus
/ dysregulated immunity
/ Endotoxemia
/ Endotoxemia - metabolism
/ Extracellular Traps
/ Gum disease
/ Humans
/ Immunity (Disease)
/ Immunology
/ Inflammation
/ inhibition of NET formation
/ Innate immunity
/ Leukocytes (neutrophilic)
/ Lipopolysaccharides
/ Lipopolysaccharides - metabolism
/ Lupus
/ NET hyper-responsiveness
/ NET-induced damage
/ neutrophil hyper-responsiveness
/ Neutrophils
/ Pathogens
/ Periodontitis
/ Periodontitis - pathology
/ Proteins
/ SARS-CoV-2
/ Severe acute respiratory syndrome coronavirus 2
/ Spike Glycoprotein, Coronavirus
/ Spike protein
/ trained immunity
2022
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Journal Article
Periodontitis-Derived Dark-NETs in Severe Covid-19
2022
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Overview
The frequent severe COVID-19 course in patients with periodontitis suggests a link of the aetiopathogenesis of both diseases. The formation of intravascular neutrophil extracellular traps (NETs) is crucial to the pathogenesis of severe COVID-19. Periodontitis is characterised by an increased level of circulating NETs, a propensity for increased NET formation, delayed NET clearance and low-grade endotoxemia (LGE). The latter has an enormous impact on innate immunity and susceptibility to infection with SARS-CoV-2. LPS binds the SARS-CoV-2 spike protein and this complex, which is more active than unbound LPS, precipitates massive NET formation. Thus, circulating NET formation is the common denominator in both COVID-19 and periodontitis and other diseases with low-grade endotoxemia like diabetes, obesity and cardiovascular diseases (CVD) also increase the risk to develop severe COVID-19. Here we discuss the role of propensity for increased NET formation, DNase I deficiency and low-grade endotoxaemia in periodontitis as aggravating factors for the severe course of COVID-19 and possible strategies for the diminution of increased levels of circulating periodontitis-derived NETs in COVID-19 with periodontitis comorbidity.
Publisher
Frontiers Media SA,Frontiers Media S.A
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