Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText.
Kick-your-searchterm to multiple Engines kick-your-query now !>
A dictionary by aggregated review articles of nephrology, medicine and the life sciences
Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

suck abstract from ncbi


10.7554/eLife.68563

http://scihub22266oqcxt.onion/10.7554/eLife.68563
suck pdf from google scholar
34866574!8709575!34866574
unlimited free pdf from europmc34866574    free
PDF from PMC    free
html from PMC    free
PDF vom PMID34866574 :   free

suck abstract from ncbi

pmid34866574
Nephropedia Template TP

gab.com Text

Twit Text FOAVip

Twit Text #

English Wikipedia


  • 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]


  • DeepDyve
  • Pubget Overpricing
  • suck abstract from ncbi

    ä ä.10 2021