BioAcyl Corp |
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| Resource type: Journal Article DOI: 10.1038/s41385-021-00482-8 ID no. (ISBN etc.): 1935-3456 BibTeX citation key: Bohnacker2022 View all bibliographic details |
Categories: BioAcyl Corp, BioAcyl Corp Subcategories: COVID-19, Inflammation resolution Creators: Bohnacker, Chaker, Erber, Esser-von Bieren, Giglberger, Hartung, Henkel, Knolle, Kolmert, Kugler, Lechner, Lingor, Pechtold, Priller, Protzer, Quaranta, Schmidt-Weber, Ud-Dean, Wheelock, Yazici Collection: Mucosal Immunology |
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| Abstract |
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Monocyte-derived macrophages (MDM) drive the inflammatory response to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and they are a major source of eicosanoids in airway inflammation. Here we report that MDM from SARS-CoV-2-infected individuals with mild disease show an inflammatory transcriptional and metabolic imprint that lasts for at least 5 months after SARS-CoV-2 infection. MDM from convalescent SARS-CoV-2-infected individuals showed a downregulation of pro-resolving factors and an increased production of pro-inflammatory eicosanoids, particularly 5-lipoxygenase-derived leukotrienes. Leukotriene synthesis was further enhanced by glucocorticoids and remained elevated at 3–5 months, but had returned to baseline at 12 months post SARS-CoV-2 infection. Stimulation with SARS-CoV-2 spike protein or LPS triggered exaggerated prostanoid-, type I IFN-, and chemokine responses in post COVID-19 MDM. Thus, SARS-CoV-2 infection leaves an inflammatory imprint in the monocyte/ macrophage compartment that drives aberrant macrophage effector functions and eicosanoid metabolism, resulting in long-term immune aberrations in patients recovering from mild COVID-19.
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| Notes |
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Added by: Dr. Enrique Feoli Last edited by: Dr. Enrique Feoli |