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Persistent Oxidative Stress and Inflammasome Activation in CD14highCD16- Monocytes From COVID-19 Patients.
Lage, Silvia Lucena; Amaral, Eduardo Pinheiro; Hilligan, Kerry L; Laidlaw, Elizabeth; Rupert, Adam; Namasivayan, Sivaranjani; Rocco, Joseph; Galindo, Frances; Kellogg, Anela; Kumar, Princy; Poon, Rita; Wortmann, Glenn W; Shannon, John P; Hickman, Heather D; Lisco, Andrea; Manion, Maura; Sher, Alan; Sereti, Irini.
  • Lage SL; HIV Pathogenesis Section, Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, United States.
  • Amaral EP; Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, United States.
  • Hilligan KL; Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, United States.
  • Laidlaw E; Immune Cell Biology Programme, Malaghan Institute of Medical Research, Wellington, New Zealand.
  • Rupert A; HIV Pathogenesis Section, Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, United States.
  • Namasivayan S; AIDS Monitoring Laboratory, Frederick National Laboratory for Cancer Research, Leidos Biomedical Research, Inc., Frederick, MD, United States.
  • Rocco J; Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, United States.
  • Galindo F; HIV Pathogenesis Section, Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, United States.
  • Kellogg A; HIV Pathogenesis Section, Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, United States.
  • Kumar P; Clinical Monitoring Research Program Directorate, Frederick National Laboratory for Cancer Research, Leidos Biomedical Research, Inc., Frederick, MD, United States.
  • Poon R; Division of Infectious Diseases and Tropical Medicine, Georgetown University Medical Center, Washington, DC, United States.
  • Wortmann GW; Division of Infectious Diseases and Travel Medicine, MedStar Georgetown University Hospital, Washington, DC, United States.
  • Shannon JP; Section of Infectious Diseases, MedStar Washington Hospital Center, Washington, DC, United States.
  • Hickman HD; Viral Immunity and Pathogenesis Unit, Laboratory of Clinical Immunology and Microbiology, National Institutes of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, United States.
  • Lisco A; Viral Immunity and Pathogenesis Unit, Laboratory of Clinical Immunology and Microbiology, National Institutes of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, United States.
  • Manion M; HIV Pathogenesis Section, Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, United States.
  • Sher A; HIV Pathogenesis Section, Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, United States.
  • Sereti I; Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, United States.
Front Immunol ; 12: 799558, 2021.
Article in English | MEDLINE | ID: covidwho-1662582
Preprint
This scientific journal article is probably based on a previously available preprint. It has been identified through a machine matching algorithm, human confirmation is still pending.
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ABSTRACT
The poor outcome of the coronavirus disease-2019 (COVID-19), caused by SARS-CoV-2, is associated with systemic hyperinflammatory response and immunopathology. Although inflammasome and oxidative stress have independently been implicated in COVID-19, it is poorly understood whether these two pathways cooperatively contribute to disease severity. Herein, we found an enrichment of CD14highCD16- monocytes displaying inflammasome activation evidenced by caspase-1/ASC-speck formation in severe COVID-19 patients when compared to mild ones and healthy controls, respectively. Those cells also showed aberrant levels of mitochondrial superoxide and lipid peroxidation, both hallmarks of the oxidative stress response, which strongly correlated with caspase-1 activity. In addition, we found that NLRP3 inflammasome-derived IL-1ß secretion by SARS-CoV-2-exposed monocytes in vitro was partially dependent on lipid peroxidation. Importantly, altered inflammasome and stress responses persisted after short-term patient recovery. Collectively, our findings suggest oxidative stress/NLRP3 signaling pathway as a potential target for host-directed therapy to mitigate early COVID-19 hyperinflammation and also its long-term outcomes.
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Full text: Available Collection: International databases Database: MEDLINE Main subject: Monocytes / Receptors, IgG / Oxidative Stress / Lipopolysaccharide Receptors / Inflammasomes / COVID-19 Type of study: Prognostic study Limits: Aged / Female / Humans / Male / Middle aged Language: English Journal: Front Immunol Year: 2021 Document Type: Article Affiliation country: Fimmu.2021.799558

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Full text: Available Collection: International databases Database: MEDLINE Main subject: Monocytes / Receptors, IgG / Oxidative Stress / Lipopolysaccharide Receptors / Inflammasomes / COVID-19 Type of study: Prognostic study Limits: Aged / Female / Humans / Male / Middle aged Language: English Journal: Front Immunol Year: 2021 Document Type: Article Affiliation country: Fimmu.2021.799558