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10.1128/mbio.00951-22

http://scihub22266oqcxt.onion/10.1128/mbio.00951-22
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35587188!9239151!35587188
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suck abstract from ncbi


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pmid35587188      mBio 2022 ; 13 (3): e0095122
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  • Circulatory Exosomes from COVID-19 Patients Trigger NLRP3 Inflammasome in Endothelial Cells #MMPMID35587188
  • Sur S; Steele R; Isbell TS; Ray R; Ray RB
  • mBio 2022[Jun]; 13 (3): e0095122 PMID35587188show ga
  • Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection induces inflammatory response, cytokine storm, venous thromboembolism, coagulopathy, and multiple organ damage. Resting endothelial cells prevent coagulation, control blood flow, and inhibit inflammation. However, it remains unknown how SARS-CoV-2 induces strong molecular signals in distant cells for immunopathogenesis. In this study, we examined the consequence of human endothelial cells, microvascular endothelial cells (HMEC-1), and liver endothelial cells (TMNK-1) to exosomes isolated from plasma of mild or severe COVID-19 patients. We observed a significant induction of NLRP3, caspase-1, and interleukin-1beta (IL-1beta) mRNA expression in endothelial cells following exposure to exosomes from severe COVID-19 patients compared with that from patients with mild disease or healthy donors. Activation of caspase-1 was noted in the endothelial cell culture medium following exposure to the COVID-19 exosomes. Furthermore, COVID-19 exosomes significantly induced mature IL-1beta secretion in both HMEC-1 and TMNK-1 endothelial cell culture medium. Thus, our results demonstrated for the first time that exosomes from COVID-19 plasma trigger NLRP3 inflammasome in endothelial cells of distant organs resulting in IL-1beta secretion and inflammatory response. IMPORTANCE Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is a global health problem. Although the vaccine controls infection, understanding the molecular mechanism of pathogenesis will help in developing future therapies. Furthermore, several investigators predicted the involvement of endothelial cell-related inflammation in SARS-CoV-2 infection and using extracellular vesicles as a cargo to carry a drug or vaccine for combating SARS-CoV-2 infection. However, the mechanism by which endothelial cells are inflamed remains unknown. Our present study highlights that exosomes from severe COVID-19 patients can enhance inflammasome activity in distant endothelial cells for augmentation of immunopathogenesis and opens an avenue for developing therapies.
  • |*COVID-19[MESH]
  • |*Exosomes/metabolism[MESH]
  • |Caspases[MESH]
  • |Endothelial Cells/metabolism[MESH]
  • |Humans[MESH]
  • |Inflammasomes/metabolism[MESH]
  • |Inflammation[MESH]
  • |NLR Family, Pyrin Domain-Containing 3 Protein/genetics/metabolism[MESH]


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