2. Academic Validation
  3. Platelets mediate inflammatory monocyte activation by SARS-CoV-2 spike protein

Platelets mediate inflammatory monocyte activation by SARS-CoV-2 spike protein

  • J Clin Invest. 2022 Feb 15;132(4):e150101. doi: 10.1172/JCI150101.
Tianyang Li 1,  Yang Yang 1,  Yongqi Li 1,  Zhengmin Wang 1,  Faxiang Ma 1,  Runqi Luo 2,  Xiaoming Xu 2,  Guo Zhou 2,  Jianhua Wang 3,  Junqi Niu 4,  Guoyue Lv 4,  Ian N Crispe 5,  Zhengkun Tu 1 4
Affiliations

Affiliations

  • 1 Institute of Translational Medicine, The First Hospital of Jilin University, Changchun, Jilin, China.
  • 2 Department of Infectious Disease, The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, China.
  • 3 Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou, Guangdong, China.
  • 4 Institute of Liver Diseases, The First Hospital of Jilin University, Changchun, Jilin, China.
  • 5 Department of Laboratory Medicine and Pathology, University of Washington, Seattle, Washington, USA.
PMID: 34964720 DOI: 10.1172/JCI150101
Abstract

Infection with SARS-CoV-2, the causative agent of COVID-19, causes mild to moderate disease in most patients but carries a risk of morbidity and mortality. Seriously affected individuals manifest disorders of hemostasis and a cytokine storm, but it is not understood how these manifestations of severe COVID-19 are linked. Here, we showed that the SARS-CoV-2 spike protein engaged the CD42b receptor to activate platelets via 2 distinct signaling pathways and promoted platelet-monocyte communication through the engagement of P Selectin/PGSL-1 and CD40L/CD40, which led to proinflammatory cytokine production by monocytes. These results explain why hypercoagulation, monocyte activation, and a cytokine storm are correlated in patients severely affected by COVID-19 and suggest a potential target for therapeutic intervention.

Keywords

COVID-19; Inflammation; Monocytes; Platelets.

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