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  • SARS-CoV-2 spike protein induces inflammation via TLR2-dependent activation of the NF-kappaB pathway #MMPMID34866574
  • Khan S; Shafiei MS; Longoria C; Schoggins JW; Savani RC; Zaki H
  • Elife 2021[Dec]; 10 (ä): ä PMID34866574show ga
  • The pathogenesis of COVID-19 is associated with a hyperinflammatory response; however, the precise mechanism of SARS-CoV-2-induced inflammation is poorly understood. Here, we investigated direct inflammatory functions of major structural proteins of SARS-CoV-2. We observed that spike (S) protein potently induced inflammatory cytokines and chemokines, including IL-6, IL-1beta, TNFalpha, CXCL1, CXCL2, and CCL2, but not IFNs in human and mouse macrophages. No such inflammatory response was observed in response to membrane (M), envelope (E), and nucleocapsid (N) proteins. When stimulated with extracellular S protein, human and mouse lung epithelial cells also produced inflammatory cytokines and chemokines. Interestingly, epithelial cells expressing S protein intracellularly were non-inflammatory, but elicited an inflammatory response in macrophages when co-cultured. Biochemical studies revealed that S protein triggers inflammation via activation of the NF-kappaB pathway in a MyD88-dependent manner. Further, such an activation of the NF-kappaB pathway was abrogated in Tlr2-deficient macrophages. Consistently, administration of S protein-induced IL-6, TNF-alpha, and IL-1beta in wild-type, but not Tlr2-deficient mice. Notably, upon recognition of S protein, TLR2 dimerizes with TLR1 or TLR6 to activate the NF-kappaB pathway. Taken together, these data reveal a mechanism for the cytokine storm during SARS-CoV-2 infection and suggest that TLR2 could be a potential therapeutic target for COVID-19.
  • |A549 Cells[MESH]
  • |Animals[MESH]
  • |HEK293 Cells[MESH]
  • |Humans[MESH]
  • |Inflammation/*virology[MESH]
  • |Mice[MESH]
  • |NF-kappa B/*physiology[MESH]
  • |SARS-CoV-2/*physiology[MESH]
  • |Signal Transduction[MESH]
  • |Spike Glycoprotein, Coronavirus/*immunology[MESH]
  • |Toll-Like Receptor 2/*genetics/metabolism[MESH]

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  • suck abstract from ncbi

    ä ä.10 2021