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10.1128/mSphere.00367-20

http://scihub22266oqcxt.onion/10.1128/mSphere.00367-20
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32581077!7316488!32581077
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suck abstract from ncbi


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pmid32581077      mSphere 2020 ; 5 (3): ä
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  • COVID-19 Hyperinflammation: What about Neutrophils? #MMPMID32581077
  • Didangelos A
  • mSphere 2020[Jun]; 5 (3): ä PMID32581077show ga
  • COVID-19 is often related to hyperinflammation that drives lung or multiorgan injury. The immunopathological mechanisms that cause excessive inflammation are under investigation and constantly updated. Here, a gene network approach was used on recently published data sets to identify possible COVID-19 inflammatory mechanisms and bioactive genes. First, network analysis of putative SARS-CoV-2 cellular receptors led to the mining of a neutrophil-response signature and relevant inflammatory genes. Second, analysis of RNA-seq data sets of lung cells infected with SARS-CoV-2 revealed that infected cells expressed neutrophil-attracting chemokines. Third, analysis of RNA-seq data sets of bronchoalveolar lavage fluid cells from COVID-19 patients identified upregulation of neutrophil genes and chemokines. Different inflammatory genes mined here, including TNFR, IL-8, CXCR1, CXCR2, ADAM10, GPR84, MME, ANPEP, and LAP3, might be druggable targets in efforts to limit SARS-CoV-2 inflammation in severe clinical cases. The possible role of neutrophils in COVID-19 inflammation needs to be studied further.
  • |Betacoronavirus/*immunology[MESH]
  • |Bronchoalveolar Lavage Fluid/cytology[MESH]
  • |COVID-19[MESH]
  • |Chemokines/genetics/*immunology[MESH]
  • |Coronavirus Infections/*immunology/pathology[MESH]
  • |Humans[MESH]
  • |Inflammation/immunology/*pathology[MESH]
  • |Lung Diseases/immunology/pathology[MESH]
  • |Neutrophil Infiltration/immunology[MESH]
  • |Neutrophils/*immunology[MESH]
  • |Pandemics[MESH]
  • |Pneumonia, Viral/*immunology/pathology[MESH]
  • |Receptors, Virus/genetics[MESH]


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