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The Defenders of the Alveolus Succumb in COVID-19 Pneumonia to SARS-CoV-2 and Necroptosis, Pyroptosis, and PANoptosis

The Journal of infectious diseases, 2023-05, Vol.227 (11), p.1245-1254 [Peer Reviewed Journal]

The Author(s) 2023. Published by Oxford University Press on behalf of Infectious Diseases Society of America. 2023 ;The Author(s) 2023. Published by Oxford University Press on behalf of Infectious Diseases Society of America. ;ISSN: 0022-1899 ;EISSN: 1537-6613 ;DOI: 10.1093/infdis/jiad056 ;PMID: 36869698

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Title:
The Defenders of the Alveolus Succumb in COVID-19 Pneumonia to SARS-CoV-2 and Necroptosis, Pyroptosis, and PANoptosis
Author: Schifanella, Luca ; Anderson, Jodi ; Wieking, Garritt ; Southern, Peter J ; Antinori, Spinello ; Galli, Massimo ; Corbellino, Mario ; Lai, Alessia ; Klatt, Nichole ; Schacker, Timothy W ; Haase, Ashley T
Subjects: Alveoli ; Apoptosis ; Bruton's tyrosine kinase ; Cell death ; Cell proliferation ; Coronaviruses ; COVID-19 ; COVID-19 - pathology ; Humans ; Inflammation ; Lung - pathology ; Major ; Necroptosis ; Pneumocytes ; Pneumonia ; Pyroptosis ; SARS-CoV-2 ; Severe acute respiratory syndrome coronavirus 2 ; Tumor necrosis factor-TNF
Is Part Of: The Journal of infectious diseases, 2023-05, Vol.227 (11), p.1245-1254
Description: Abstract Alveolar type II (ATII) pneumocytes as defenders of the alveolus are critical to repairing lung injury. We investigated the ATII reparative response in coronavirus disease 2019 (COVID-19) pneumonia, because the initial proliferation of ATII cells in this reparative process should provide large numbers of target cells to amplify severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus production and cytopathological effects to compromise lung repair. We show that both infected and uninfected ATII cells succumb to tumor necrosis factor-α (TNF)-induced necroptosis, Bruton tyrosine kinase (BTK)-induced pyroptosis, and a new PANoptotic hybrid form of inflammatory cell death mediated by a PANoptosomal latticework that generates distinctive COVID-19 pathologies in contiguous ATII cells. Identifying TNF and BTK as the initiators of programmed cell death and SARS-CoV-2 cytopathic effects provides a rationale for early antiviral treatment combined with inhibitors of TNF and BTK to preserve ATII cell populations, reduce programmed cell death and associated hyperinflammation, and restore functioning alveoli in COVID-19 pneumonia. Death in fatal COVID-19 pneumonia of SARS-CoV-2 infected and uninfected ATII pneumocytes is mediated by autochthonous expression of TNF-induced necroptic, BTK-induced pyroptotic, and apoptotic pathways in ATII cell PANoptosomes.
Publisher: United States: Oxford University Press
Language: English
Identifier: ISSN: 0022-1899
EISSN: 1537-6613
DOI: 10.1093/infdis/jiad056
PMID: 36869698
Source: Geneva Foundation Free Medical Journals at publisher websites
MEDLINE
Alma/SFX Local Collection
Oxford Academic Journals (Open Access)

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The Defenders of the Alveolus Succumb in COVID-19 Pneumonia to SARS-CoV-2 and Necroptosis, Pyroptosis, and PANoptosis

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