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10.1016/j.intimp.2021.108201

http://scihub22266oqcxt.onion/10.1016/j.intimp.2021.108201
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suck abstract from ncbi


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pmid34653729      Int+Immunopharmacol 2021 ; 101 (Pt B): 108201
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  • In vitro induction of interleukin-8 by SARS-CoV-2 Spike protein is inhibited in bronchial epithelial IB3-1 cells by a miR-93-5p agomiR #MMPMID34653729
  • Gasparello J; d'Aversa E; Breveglieri G; Borgatti M; Finotti A; Gambari R
  • Int Immunopharmacol 2021[Dec]; 101 (Pt B): 108201 PMID34653729show ga
  • One of the major clinical features of COVID-19 is a hyperinflammatory state, which is characterized by high expression of cytokines (such as IL-6 and TNF-alpha), chemokines (such as IL-8) and growth factors and is associated with severe forms of COVID-19. For this reason, the control of the "cytokine storm" represents a key issue in the management of COVID-19 patients. In this study we report evidence that the release of key proteins of the COVID-19 "cytokine storm" can be inhibited by mimicking the biological activity of microRNAs. The major focus of this report is on IL-8, whose expression can be modified by the employment of a molecule mimicking miR-93-5p, which is able to target the IL-8 RNA transcript and modulate its activity. The results obtained demonstrate that the production of IL-8 protein is enhanced in bronchial epithelial IB3-1 cells by treatment with the SARS-CoV-2 Spike protein and that IL-8 synthesis and extracellular release can be strongly reduced using an agomiR molecule mimicking miR-93-5p.
  • |*MicroRNAs[MESH]
  • |Bronchi/cytology[MESH]
  • |Cell Line[MESH]
  • |Epithelial Cells/*immunology[MESH]
  • |Humans[MESH]
  • |Interleukin-8/genetics/*immunology[MESH]


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