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10.3389/fimmu.2021.683800

http://scihub22266oqcxt.onion/10.3389/fimmu.2021.683800
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suck abstract from ncbi


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pmid34248968      Front+Immunol 2021 ; 12 (ä): 683800
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  • SARS-CoV-2/ACE2 Interaction Suppresses IRAK-M Expression and Promotes Pro-Inflammatory Cytokine Production in Macrophages #MMPMID34248968
  • Pantazi I; Al-Qahtani AA; Alhamlan FS; Alothaid H; Matou-Nasri S; Sourvinos G; Vergadi E; Tsatsanis C
  • Front Immunol 2021[]; 12 (ä): 683800 PMID34248968show ga
  • The major cause of death in SARS-CoV-2 infected patients is due to de-regulation of the innate immune system and development of cytokine storm. SARS-CoV-2 infects multiple cell types in the lung, including macrophages, by engagement of its spike (S) protein on angiotensin converting enzyme 2 (ACE2) receptor. ACE2 receptor initiates signals in macrophages that modulate their activation, including production of cytokines and chemokines. IL-1R-associated kinase (IRAK)-M is a central regulator of inflammatory responses regulating the magnitude of TLR responsiveness. Aim of the work was to investigate whether SARS-CoV-2 S protein-initiated signals modulate pro-inflammatory cytokine production in macrophages. For this purpose, we treated PMA-differentiated THP-1 human macrophages with SARS-CoV-2 S protein and measured the induction of inflammatory mediators including IL6, TNFalpha, IL8, CXCL5, and MIP1a. The results showed that SARS-CoV-2 S protein induced IL6, MIP1a and TNFalpha mRNA expression, while it had no effect on IL8 and CXCL5 mRNA levels. We further examined whether SARS-CoV-2 S protein altered the responsiveness of macrophages to TLR signals. Treatment of LPS-activated macrophages with SARS-CoV-2 S protein augmented IL6 and MIP1a mRNA, an effect that was evident at the protein level only for IL6. Similarly, treatment of PAM3csk4 stimulated macrophages with SARS-CoV-2 S protein resulted in increased mRNA of IL6, while TNFalpha and MIP1a were unaffected. The results were confirmed in primary human peripheral monocytic cells (PBMCs) and isolated CD14+ monocytes. Macrophage responsiveness to TLR ligands is regulated by IRAK-M, an inactive IRAK kinase isoform. Indeed, we found that SARS-CoV-2 S protein suppressed IRAK-M mRNA and protein expression both in THP1 macrophages and primary human PBMCs and CD14+ monocytes. Engagement of SARS-CoV-2 S protein with ACE2 results in internalization of ACE2 and suppression of its activity. Activation of ACE2 has been previously shown to induce anti-inflammatory responses in macrophages. Treatment of macrophages with the ACE2 activator DIZE suppressed the pro-inflammatory action of SARS-CoV-2. Our results demonstrated that SARS-CoV-2/ACE2 interaction rendered macrophages hyper-responsive to TLR signals, suppressed IRAK-M and promoted pro-inflammatory cytokine expression. Thus, activation of ACE2 may be a potential anti-inflammatory therapeutic strategy to eliminate the development of cytokine storm observed in COVID-19 patients.
  • |Adaptor Proteins, Signal Transducing/genetics/metabolism[MESH]
  • |Angiotensin-Converting Enzyme 2/*metabolism[MESH]
  • |COVID-19/*immunology[MESH]
  • |Cytokine Release Syndrome/*immunology[MESH]
  • |Gene Expression Regulation[MESH]
  • |Humans[MESH]
  • |Immunity, Innate[MESH]
  • |Inflammation Mediators/metabolism[MESH]
  • |Interleukin-1 Receptor-Associated Kinases/genetics/*metabolism[MESH]
  • |Interleukin-6/genetics/metabolism[MESH]
  • |Lipopolysaccharides/immunology[MESH]
  • |Macrophages/*immunology/virology[MESH]
  • |Protein Binding[MESH]
  • |SARS-CoV-2/*physiology[MESH]
  • |Spike Glycoprotein, Coronavirus/*metabolism[MESH]
  • |THP-1 Cells[MESH]


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