Thromboinflammation Supports Complement Activation in Cancer Patients With COVID-19.


Journal

Frontiers in immunology
ISSN: 1664-3224
Titre abrégé: Front Immunol
Pays: Switzerland
ID NLM: 101560960

Informations de publication

Date de publication:
2021
Historique:
received: 28 05 2021
accepted: 02 08 2021
entrez: 7 9 2021
pubmed: 8 9 2021
medline: 21 9 2021
Statut: epublish

Résumé

COVID-19 pathology is associated with exuberant inflammation, vascular damage, and activation of coagulation. In addition, complement activation has been described and is linked to disease pathology. However, few studies have been conducted in cancer patients. This study examined complement activation in response to COVID-19 in the setting of cancer associated thromboinflammation. Markers of complement activation (C3a, C5a, sC5b-9) and complement inhibitors (Factor H, C1-Inhibitor) were evaluated in plasma of cancer patients with (n=43) and without (n=43) COVID-19 and stratified based on elevated plasma D-dimer levels (>1.0 μg/ml FEU). Markers of vascular endothelial cell dysfunction and platelet activation (ICAM-1, thrombomodulin, P-selectin) as well as systemic inflammation (pentraxin-3, serum amyloid A, soluble urokinase plasminogen activator receptor) were analyzed to further evaluate the inflammatory response. Increases in circulating markers of endothelial cell dysfunction, platelet activation, and systemic inflammation were noted in cancer patients with COVID-19. In contrast, complement activation increased in cancer patients with COVID-19 and elevated D-dimers. This was accompanied by decreased C1-Inhibitor levels in patients with D-dimers > 5 ug/ml FEU. Complement activation in cancer patients with COVID-19 is significantly increased in the setting of thromboinflammation. These findings support a link between coagulation and complement cascades in the setting of inflammation.

Sections du résumé

Background
COVID-19 pathology is associated with exuberant inflammation, vascular damage, and activation of coagulation. In addition, complement activation has been described and is linked to disease pathology. However, few studies have been conducted in cancer patients.
Objective
This study examined complement activation in response to COVID-19 in the setting of cancer associated thromboinflammation.
Methods
Markers of complement activation (C3a, C5a, sC5b-9) and complement inhibitors (Factor H, C1-Inhibitor) were evaluated in plasma of cancer patients with (n=43) and without (n=43) COVID-19 and stratified based on elevated plasma D-dimer levels (>1.0 μg/ml FEU). Markers of vascular endothelial cell dysfunction and platelet activation (ICAM-1, thrombomodulin, P-selectin) as well as systemic inflammation (pentraxin-3, serum amyloid A, soluble urokinase plasminogen activator receptor) were analyzed to further evaluate the inflammatory response.
Results
Increases in circulating markers of endothelial cell dysfunction, platelet activation, and systemic inflammation were noted in cancer patients with COVID-19. In contrast, complement activation increased in cancer patients with COVID-19 and elevated D-dimers. This was accompanied by decreased C1-Inhibitor levels in patients with D-dimers > 5 ug/ml FEU.
Conclusion
Complement activation in cancer patients with COVID-19 is significantly increased in the setting of thromboinflammation. These findings support a link between coagulation and complement cascades in the setting of inflammation.

Identifiants

pubmed: 34491250
doi: 10.3389/fimmu.2021.716361
pmc: PMC8416543
doi:

Substances chimiques

Biomarkers 0
Complement Inactivating Agents 0
Fibrin Fibrinogen Degradation Products 0
fibrin fragment D 0

Types de publication

Journal Article Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

716361

Subventions

Organisme : NCI NIH HHS
ID : P30 CA008748
Pays : United States

Informations de copyright

Copyright © 2021 Peerschke, Valentino, So, Shulman and Ravinder.

Déclaration de conflit d'intérêts

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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Auteurs

Ellinor I Peerschke (EI)

Department of Laboratory Medicine, Memorial Sloan Kettering Cancer Center, New York, NY, United States.

Alisa Valentino (A)

Department of Laboratory Medicine, Memorial Sloan Kettering Cancer Center, New York, NY, United States.

Rachel J So (RJ)

Department of Laboratory Medicine, Memorial Sloan Kettering Cancer Center, New York, NY, United States.

Scott Shulman (S)

Department of Laboratory Medicine, Memorial Sloan Kettering Cancer Center, New York, NY, United States.
Department of Laboratory Medicine, Memorial Sloan Kettering Cancer Center, New York, NY, United States.

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Classifications MeSH