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10.1093/jmcb/mjaa067

http://scihub22266oqcxt.onion/10.1093/jmcb/mjaa067
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33295606!7799037!33295606
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suck abstract from ncbi


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pmid33295606      J+Mol+Cell+Biol 2020 ; 12 (12): 916-932
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  • SARS-CoV-2 spike protein binds to bacterial lipopolysaccharide and boosts proinflammatory activity #MMPMID33295606
  • Petruk G; Puthia M; Petrlova J; Samsudin F; Stromdahl AC; Cerps S; Uller L; Kjellstrom S; Bond PJ; Schmidtchen AA
  • J Mol Cell Biol 2020[Oct]; 12 (12): 916-932 PMID33295606show ga
  • There is a link between high lipopolysaccharide (LPS) levels in the blood and the metabolic syndrome, and metabolic syndrome predisposes patients to severe COVID-19. Here, we define an interaction between SARS-CoV-2 spike (S) protein and LPS, leading to aggravated inflammation in vitro and in vivo. Native gel electrophoresis demonstrated that SARS-CoV-2 S protein binds to LPS. Microscale thermophoresis yielded a KD of approximately 47 nM for the interaction. Computational modeling and all-atom molecular dynamics simulations further substantiated the experimental results, identifying a main LPS-binding site in SARS-CoV-2 S protein. S protein, when combined with low levels of LPS, boosted nuclear factor-kappa B (NF-kappaB) activation in monocytic THP-1 cells and cytokine responses in human blood and peripheral blood mononuclear cells, respectively. The in vitro inflammatory response was further validated by employing NF-kappaB reporter mice and in vivo bioimaging. Dynamic light scattering, transmission electron microscopy, and LPS-FITC analyses demonstrated that S protein modulated the aggregation state of LPS, providing a molecular explanation for the observed boosting effect. Taken together, our results provide an interesting molecular link between excessive inflammation during infection with SARS-CoV-2 and comorbidities involving increased levels of bacterial endotoxins.
  • |*SARS-CoV-2/immunology/pathogenicity/physiology[MESH]
  • |Animals[MESH]
  • |Binding Sites[MESH]
  • |COVID-19/*complications/immunology/virology[MESH]
  • |Cytokine Release Syndrome/etiology/immunology[MESH]
  • |Disease Models, Animal[MESH]
  • |Gram-Negative Bacterial Infections/complications/immunology[MESH]
  • |Humans[MESH]
  • |In Vitro Techniques[MESH]
  • |Inflammation/*etiology[MESH]
  • |Lipid A/chemistry/immunology/metabolism[MESH]
  • |Lipopolysaccharides/chemistry/immunology/*metabolism[MESH]
  • |Mice[MESH]
  • |Mice, Inbred BALB C[MESH]
  • |Mice, Transgenic[MESH]
  • |Models, Immunological[MESH]
  • |Models, Molecular[MESH]
  • |Molecular Docking Simulation[MESH]
  • |Protein Binding[MESH]
  • |Protein Interaction Domains and Motifs[MESH]
  • |Respiratory Distress Syndrome/etiology[MESH]
  • |Risk Factors[MESH]


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