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

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 sever...

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Detalles Bibliográficos
Autores principales: Li, Tianyang, Yang, Yang, Li, Yongqi, Wang, Zhengmin, Ma, Faxiang, Luo, Runqi, Xu, Xiaoming, Zhou, Guo, Wang, Jianhua, Niu, Junqi, Lv, Guoyue, Crispe, Ian N., Tu, Zhengkun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: American Society for Clinical Investigation 2022
Materias:
Research Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8843740/
https://www.ncbi.nlm.nih.gov/pubmed/34964720
http://dx.doi.org/10.1172/JCI150101
Descripción
Sumario: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.

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