About: Glycyrrhizin inhibits highly pathogenic H5N1 influenza A virus-induced pro-inflammatory cytokine and chemokine expression in human macrophages

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About: Glycyrrhizin inhibits highly pathogenic H5N1 influenza A virus-induced pro-inflammatory cytokine and chemokine expression in human macrophages Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Glycyrrhizin inhibits highly pathogenic H5N1 influenza A virus-induced pro-inflammatory cytokine and chemokine expression in human macrophages
Creator	Cinatl, Jindrich Michaelis, Martin Altenbrandt, Behric Geiler, Janina Leutz, Anke Naczk, Patrizia Ogbomo, Henry Sithisarn, Patchima Doerr, Wilhelm Hans, •
topic	covid:5c8e04248bdaa59a4f1874291bf324d7c0182676#this
Source	Medline; PMC
abstract	Hypercytokinaemia is thought to contribute to highly pathogenic H5N1 influenza A virus disease. Glycyrrhizin is known to exert immunomodulatory and anti-inflammatory effects and therefore a candidate drug for the control of H5N1-induced pro-inflammatory gene expression. Here, the effects of an approved parenteral glycyrrhizin preparation were investigated on H5N1 virus replication, H5N1-induced pro-inflammatory responses, and H5N1-induced apoptosis in human monocyte-derived macrophages. Glycyrrhizin 100 μg/ml, a therapeutically achievable concentration, impaired H5N1-induced production of CXCL10, interleukin 6, and CCL5 and inhibited H5N1-induced apoptosis but did not interfere with H5N1 replication. Global inhibition of immune responses may result in the loss of control of virus replication by cytotoxic immune cells including natural killer cells and cytotoxic CD8(+) T-lymphocytes. Notably, glycyrrhizin concentrations that inhibited H5N1-induced pro-inflammatory gene expression did not affect cytolytic activity of natural killer cells. Since H5N1-induced hypercytokinaemia is considered to play an important role within H5N1 pathogenesis, glycyrrhizin may complement the arsenal of potential drugs for the treatment of H5N1 disease.
has issue date	2010-04-13(xsd:dateTime)
bibo:doi	10.1007/s00430-010-0155-0
bibo:pmid	20386921
has license	no-cc
sha1sum (hex)	5c8e04248bdaa59a4f1874291bf324d7c0182676
schema:url	https://doi.org/10.1007/s00430-010-0155-0
resource representing a document's title	Glycyrrhizin inhibits highly pathogenic H5N1 influenza A virus-induced pro-inflammatory cytokine and chemokine expression in human macrophages
has PubMed Central identifier	PMC7087222
has PubMed identifier	20386921
schema:publication	Med Microbiol Immunol
resource representing a document's body	covid:5c8e04248bdaa59a4f1874291bf324d7c0182676#body_text
is http://vocab.deri.ie/void#inDataset of	proxy:http/ns.inria.fr/covid19/5c8e04248bdaa59a4f1874291bf324d7c0182676
is schema:about of	named entity 'disease' named entity 'Since' named entity 'natural killer cells' named entity 'immune cells' named entity 'induced' named entity 'cytotoxic' named entity 'influenza A virus' named entity 'investigated' named entity 'gene' named entity 'human' named entity 'influenza A' named entity 'HUMAN' named entity 'TREATMENT' named entity 'INHIBITED' named entity 'GLOBAL' named entity 'CONTRIBUTE ' named entity 'CYTOTOXIC' named entity 'CCL5' named entity 'BUT' named entity 'PRO-INFLAMMATORY RESPONSES' named entity 'DISEASE' named entity 'PRO-' named entity 'COMPLEMENT' named entity 'CONCENTRATION' named entity 'APOPTOSIS' named entity 'HUMAN MONOCYTE' named entity 'HIGHLY' named entity 'INHIBITION' named entity 'NATURAL KILLER CELLS' named entity 'CD8' named entity 'INFLAMMATORY' named entity 'CONSIDERED' named entity 'INCLUDING' named entity 'THOUGHT' named entity 'IMMUNOMODULATORY' named entity 'APPROVED' named entity 'H5N1 VIRUS' named entity 'GLYCYRRHIZIN' named entity 'CHEMOKINE' named entity 'CXCL10' named entity 'ANTIINFLAMMATORY' named entity 'KNOWN' named entity 'PATHOGENIC' named entity 'PATHOGENIC' named entity 'MACROPHAGES' named entity 'EXPRESSION' named entity 'HYPERCYTOKINAEMIA' named entity 'INVESTIGATED' named entity 'INFLUENZA A VIRUS' named entity 'CYTOKINE ' named entity 'INDUCED' named entity 'MACROPHAGES' named entity 'DRUGS' named entity 'RESULT' named entity 'PRODUCTION' named entity 'DID' named entity 'DERIVED' named entity 'GENE EXPRESSION' named entity 'PREPARATION' named entity 'INTERLEUKIN 6' named entity 'AFFECT' named entity 'CONTROL' named entity 'IMMUNE CELLS' named entity 'PARENTERAL' named entity 'DRUG' named entity 'LOSS OF' named entity 'H5N1 INFLUENZA' named entity '100' named entity 'EXERT' named entity 'HERE'

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