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10.1007/s12035-021-02593-6

http://scihub22266oqcxt.onion/10.1007/s12035-021-02593-6
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34709564!8551352!34709564
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suck abstract from ncbi


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pmid34709564      Mol+Neurobiol 2022 ; 59 (1): 445-458
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  • SARS-CoV-2 Spike Glycoprotein S1 Induces Neuroinflammation in BV-2 Microglia #MMPMID34709564
  • Olajide OA; Iwuanyanwu VU; Adegbola OD; Al-Hindawi AA
  • Mol Neurobiol 2022[Jan]; 59 (1): 445-458 PMID34709564show ga
  • In addition to respiratory complications produced by SARS-CoV-2, accumulating evidence suggests that some neurological symptoms are associated with the disease caused by this coronavirus. In this study, we investigated the effects of the SARS-CoV-2 spike protein S1 stimulation on neuroinflammation in BV-2 microglia. Analyses of culture supernatants revealed an increase in the production of TNF-alpha, IL-6, IL-1beta and iNOS/NO. S1 also increased protein levels of phospho-p65 and phospho-IkappaBalpha, as well as enhanced DNA binding and transcriptional activity of NF-kappaB. These effects of the protein were blocked in the presence of BAY11-7082 (1 microM). Exposure of S1 to BV-2 microglia also increased the protein levels of NLRP3 inflammasome and enhanced caspase-1 activity. Increased protein levels of p38 MAPK was observed in BV-2 microglia stimulated with the spike protein S1 (100 ng/ml), an action that was reduced in the presence of SKF 86,002 (1 microM). Results of immunofluorescence microscopy showed an increase in TLR4 protein expression in S1-stimulated BV-2 microglia. Furthermore, pharmacological inhibition with TAK 242 (1 microM) and transfection with TLR4 small interfering RNA resulted in significant reduction in TNF-alpha and IL-6 production in S1-stimulated BV-2 microglia. These results have provided the first evidence demonstrating S1-induced neuroinflammation in BV-2 microglia. We propose that induction of neuroinflammation by this protein in the microglia is mediated through activation of NF-kappaB and p38 MAPK, possibly as a result of TLR4 activation. These results contribute to our understanding of some of the mechanisms involved in CNS pathologies of SARS-CoV-2.
  • |Animals[MESH]
  • |Caspase 1/metabolism[MESH]
  • |Cell Line[MESH]
  • |Furans/pharmacology[MESH]
  • |Indenes/pharmacology[MESH]
  • |Inflammasomes/metabolism[MESH]
  • |Interleukin-1beta/genetics[MESH]
  • |Interleukin-6/metabolism[MESH]
  • |Mice[MESH]
  • |Microglia/*metabolism/pathology[MESH]
  • |NF-kappa B/metabolism[MESH]
  • |Neuroinflammatory Diseases/pathology/*virology[MESH]
  • |Nitric Oxide Synthase Type II/metabolism[MESH]
  • |Nitric Oxide/metabolism[MESH]
  • |Nitriles/pharmacology[MESH]
  • |RNA, Small Interfering[MESH]
  • |Recombinant Proteins/metabolism[MESH]
  • |Spike Glycoprotein, Coronavirus/*metabolism[MESH]
  • |Sulfonamides/pharmacology[MESH]
  • |Sulfones/pharmacology[MESH]
  • |Toll-Like Receptor 4/metabolism[MESH]
  • |Tumor Necrosis Factor-alpha/metabolism[MESH]


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