A virus-specific monocyte inflammatory phenotype is induced by SARS-CoV-2 at the immune-epithelial interface.

Szczegóły
Abstrakt

Tytuł:: A virus-specific monocyte inflammatory phenotype is induced by SARS-CoV-2 at the immune-epithelial interface.
Autorzy:: Leon J; Department of Immunology, Blavatnik Institute, Harvard Medical School, Boston, MA 02115.; INSERM UMR 1163, University of Paris, Institut Imagine, 75015 Paris, France.
Michelson DA; Department of Immunology, Blavatnik Institute, Harvard Medical School, Boston, MA 02115.
Olejnik J; Department of Microbiology, Boston University School of Medicine, Boston, MA 02118.; National Emerging Infectious Diseases Laboratories, Boston University, Boston, MA 02215.
Chowdhary K; Department of Immunology, Blavatnik Institute, Harvard Medical School, Boston, MA 02115.
Oh HS; Department of Microbiology, Blavatnik Institute, Harvard Medical School, Boston, MA 02115.
Hume AJ; Department of Microbiology, Boston University School of Medicine, Boston, MA 02118.; National Emerging Infectious Diseases Laboratories, Boston University, Boston, MA 02215.
Galván-Peña S; Department of Immunology, Blavatnik Institute, Harvard Medical School, Boston, MA 02115.
Zhu Y; Department of Immunology, Blavatnik Institute, Harvard Medical School, Boston, MA 02115.
Chen F; Department of Immunology, Blavatnik Institute, Harvard Medical School, Boston, MA 02115.
Vijaykumar B; Department of Immunology, Blavatnik Institute, Harvard Medical School, Boston, MA 02115.
Yang L; Department of Immunology, Blavatnik Institute, Harvard Medical School, Boston, MA 02115.
Crestani E; Division of Immunology, Boston Children's Hospital, Harvard Medical School, Boston, MA 02115.; Department of Pediatrics, Harvard Medical School, Boston, MA 02115.
Yonker LM; Department of Pediatrics, Massachusetts General Hospital, Boston, MA 02114.
Knipe DM; Department of Microbiology, Blavatnik Institute, Harvard Medical School, Boston, MA 02115.
Mühlberger E; Department of Microbiology, Boston University School of Medicine, Boston, MA 02118.; National Emerging Infectious Diseases Laboratories, Boston University, Boston, MA 02215.
Benoist C; Department of Immunology, Blavatnik Institute, Harvard Medical School, Boston, MA 02115; .
Źródło:: Proceedings of the National Academy of Sciences of the United States of America [Proc Natl Acad Sci U S A] 2022 Jan 04; Vol. 119 (1).
Typ publikacji:: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
Język:: English
Imprint Name(s):: Original Publication: Washington, DC : National Academy of Sciences
MeSH Terms:: COVID-19/*immunology
Epithelial Cells/*immunology
Monocytes/*immunology
SARS-CoV-2/*pathogenicity
Adult ; B-Lymphocytes/immunology ; COVID-19/pathology ; Child ; Coculture Techniques ; Ebolavirus/pathogenicity ; Epithelial Cells/virology ; Gene Expression Profiling ; Humans ; Inflammation ; Influenza A virus/pathogenicity ; Lung/immunology ; Myeloid Cells/immunology ; Species Specificity ; Viral Proteins/immunology
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Grant Information:: R21 AI135912 United States AI NIAID NIH HHS; T32 GM007753 United States GM NIGMS NIH HHS; P01 AI098681 United States AI NIAID NIH HHS; R24 AI072073 United States AI NIAID NIH HHS; R01 AI133486 United States AI NIAID NIH HHS
Contributed Indexing:: Keywords: COVID-19; cytokine storm; interferon
Substance Nomenclature:: 0 (Viral Proteins)
Entry Date(s):: Date Created: 20211231 Date Completed: 20220117 Latest Revision: 20220127
Update Code:: 20240104
PubMed Central ID:: PMC8740714
DOI:: 10.1073/pnas.2116853118
PMID:: 34969849
: Czasopismo naukowe

Infection by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) provokes a potentially fatal pneumonia with multiorgan failure, and high systemic inflammation. To gain mechanistic insight and ferret out the root of this immune dysregulation, we modeled, by in vitro coculture, the interactions between infected epithelial cells and immunocytes. A strong response was induced in monocytes and B cells, with a SARS-CoV-2-specific inflammatory gene cluster distinct from that seen in influenza A or Ebola virus-infected cocultures, and which reproduced deviations reported in blood or lung myeloid cells from COVID-19 patients. A substantial fraction of the effect could be reproduced after individual transfection of several SARS-CoV-2 proteins (Spike and some nonstructural proteins), mediated by soluble factors, but not via transcriptional induction. This response was greatly muted in monocytes from healthy children, perhaps a clue to the age dependency of COVID-19. These results suggest that the inflammatory malfunction in COVID-19 is rooted in the earliest perturbations that SARS-CoV-2 induces in epithelia.
(Copyright © 2021 the Author(s). Published by PNAS.)

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