Caspases and therapeutic potential of caspase inhibitors in moderate-severe SARS-CoV-2 infection and long COVID.


Journal

Allergy
ISSN: 1398-9995
Titre abrégé: Allergy
Pays: Denmark
ID NLM: 7804028

Informations de publication

Date de publication:
01 2022
Historique:
revised: 21 04 2021
received: 17 02 2021
accepted: 22 04 2021
pubmed: 17 5 2021
medline: 5 1 2022
entrez: 16 5 2021
Statut: ppublish

Résumé

COVID-19 can present with lymphopenia and extraordinary complex multiorgan pathologies that can trigger long-term sequela. Given that inflammasome products, like caspase-1, play a role in the pathophysiology of a number of co-morbid conditions, we investigated caspases across the spectrum of COVID-19 disease. We assessed transcriptional states of multiple caspases and using flow cytometry, the expression of active caspase-1 in blood cells from COVID-19 patients in acute and convalescent stages of disease. Non-COVID-19 subject presenting with various comorbid conditions served as controls. Single-cell RNA-seq data of immune cells from COVID-19 patients showed a distinct caspase expression pattern in T cells, neutrophils, dendritic cells, and eosinophils compared with controls. Caspase-1 was upregulated in CD4+ T-cells from hospitalized COVID-19 patients compared with unexposed controls. Post-COVID-19 patients with lingering symptoms (long-haulers) also showed upregulated caspase-1activity in CD4+ T-cells that ex vivo was attenuated with a select pan-caspase inhibitor. We observed elevated caspase-3/7levels in red blood cells from COVID-19 patients compared with controls that was reduced following caspase inhibition. Our preliminary results suggest an exuberant caspase response in COVID-19 that may facilitate immune-related pathological processes leading to severe outcomes. Further clinical correlations of caspase expression in different stages of COVID-19 will be needed. Pan-caspase inhibition could emerge as a therapeutic strategy to ameliorate or prevent severe COVID-19.

Sections du résumé

BACKGROUND
COVID-19 can present with lymphopenia and extraordinary complex multiorgan pathologies that can trigger long-term sequela.
AIMS
Given that inflammasome products, like caspase-1, play a role in the pathophysiology of a number of co-morbid conditions, we investigated caspases across the spectrum of COVID-19 disease.
MATERIALS & METHODS
We assessed transcriptional states of multiple caspases and using flow cytometry, the expression of active caspase-1 in blood cells from COVID-19 patients in acute and convalescent stages of disease. Non-COVID-19 subject presenting with various comorbid conditions served as controls.
RESULTS
Single-cell RNA-seq data of immune cells from COVID-19 patients showed a distinct caspase expression pattern in T cells, neutrophils, dendritic cells, and eosinophils compared with controls. Caspase-1 was upregulated in CD4+ T-cells from hospitalized COVID-19 patients compared with unexposed controls. Post-COVID-19 patients with lingering symptoms (long-haulers) also showed upregulated caspase-1activity in CD4+ T-cells that ex vivo was attenuated with a select pan-caspase inhibitor. We observed elevated caspase-3/7levels in red blood cells from COVID-19 patients compared with controls that was reduced following caspase inhibition.
DISCUSSION
Our preliminary results suggest an exuberant caspase response in COVID-19 that may facilitate immune-related pathological processes leading to severe outcomes. Further clinical correlations of caspase expression in different stages of COVID-19 will be needed.
CONCLUSION
Pan-caspase inhibition could emerge as a therapeutic strategy to ameliorate or prevent severe COVID-19.

Identifiants

pubmed: 33993490
doi: 10.1111/all.14907
pmc: PMC8222863
doi:

Substances chimiques

Caspase Inhibitors 0
CASP3 protein, human EC 3.4.22.-
CASP7 protein, human EC 3.4.22.-
Caspase 3 EC 3.4.22.-
Caspase 7 EC 3.4.22.-
Caspases EC 3.4.22.-
Caspase 1 EC 3.4.22.36

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

118-129

Subventions

Organisme : NHLBI NIH HHS
ID : K01 HL140271
Pays : United States

Informations de copyright

© 2021 European Academy of Allergy and Clinical Immunology and John Wiley & Sons Ltd.

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Auteurs

Matthew Plassmeyer (M)

Amerimmune, Fairfax, VA, USA.

Oral Alpan (O)

Amerimmune, Fairfax, VA, USA.

Michael J Corley (MJ)

Department of Medicine, Division of Infectious Diseases, Weill Cornell Medicine, New York City, NY, USA.

Thomas A Premeaux (TA)

Department of Medicine, Division of Infectious Diseases, Weill Cornell Medicine, New York City, NY, USA.

Kimberleigh Lillard (K)

Amerimmune, Fairfax, VA, USA.

Paige Coatney (P)

Amerimmune, Fairfax, VA, USA.

Tina Vaziri (T)

Amerimmune, Fairfax, VA, USA.

Suzan Michalsky (S)

Amerimmune, Fairfax, VA, USA.

Alina P S Pang (APS)

Department of Medicine, Division of Infectious Diseases, Weill Cornell Medicine, New York City, NY, USA.

Zaheer Bukhari (Z)

S.U.N.Y. Downstate Health Sciences University, Brooklyn, NY, USA.

Stephen T Yeung (ST)

Department of Medicine, Division of Infectious Diseases, Weill Cornell Medicine, New York City, NY, USA.

Teresa H Evering (TH)

Department of Medicine, Division of Infectious Diseases, Weill Cornell Medicine, New York City, NY, USA.

Gail Naughton (G)

Histogen, Inc, San Diego, CA, USA.

Martin Latterich (M)

Histogen, Inc, San Diego, CA, USA.

Philip Mudd (P)

Department of Emergency Medicine, Washington University School of Medicine, Saint Louis, MO, USA.

Alfred Spada (A)

Histogen, Inc, San Diego, CA, USA.

Nicole Rindone (N)

Histogen, Inc, San Diego, CA, USA.

Denise Loizou (D)

Histogen, Inc, San Diego, CA, USA.

Søren Ulrik Sønder (S)

Amerimmune, Fairfax, VA, USA.

Lishomwa C Ndhlovu (LC)

Department of Medicine, Division of Infectious Diseases, Weill Cornell Medicine, New York City, NY, USA.

Raavi Gupta (R)

S.U.N.Y. Downstate Health Sciences University, Brooklyn, NY, USA.

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Classifications MeSH