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http://purl.uniprot.org/citations/26967533http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/26967533http://www.w3.org/2000/01/rdf-schema#comment"Interleukin 1 (IL-1) β is a critical cytokine that orchestrates host defenses against Staphylococcus aureus and is crucial for the eradication of bacteria. The production and action of IL-1β are regulated by multiple control pathways. Among them, IL-1RII (the type II IL-1 receptor) acts as a decoy receptor and has been shown to regulate the biological effects of IL-1β. High levels of soluble IL-1RII are present in septic patients; however, the stimuli that regulate the expression and release of IL-1RII in pathological conditions are incompletely elucidated. In the present study, we demonstrated the ability of S. aureus and protein A to induce IL-1RII shedding in myeloid cells. The positive modulation of IL-1RII expression and cleavage was associated with the failure to detect IL-1β in response to S. aureus both in vitro and in vivo, suggesting that the soluble form of the receptor could be masking the availability of IL-1β. The absence of detectable IL-1β was associated with low levels of inflammatory cytokines and chemokines known to be regulated by IL-1β and with increased bacterial persistence. Modulation of decoy receptors during systemic S. aureus infection is proposed as a new strategy used by this bacterium to evade the immune response."xsd:string
http://purl.uniprot.org/citations/26967533http://purl.org/dc/terms/identifier"doi:10.1159/000443663"xsd:string
http://purl.uniprot.org/citations/26967533http://purl.uniprot.org/core/author"Sordelli D.O."xsd:string
http://purl.uniprot.org/citations/26967533http://purl.uniprot.org/core/author"Garofalo A."xsd:string
http://purl.uniprot.org/citations/26967533http://purl.uniprot.org/core/author"Gomez M.I."xsd:string
http://purl.uniprot.org/citations/26967533http://purl.uniprot.org/core/author"Gonzalez C.D."xsd:string
http://purl.uniprot.org/citations/26967533http://purl.uniprot.org/core/author"Ojeda D."xsd:string
http://purl.uniprot.org/citations/26967533http://purl.uniprot.org/core/author"Trevani A.S."xsd:string
http://purl.uniprot.org/citations/26967533http://purl.uniprot.org/core/author"Giai C."xsd:string
http://purl.uniprot.org/citations/26967533http://purl.uniprot.org/core/author"Sabbione F."xsd:string
http://purl.uniprot.org/citations/26967533http://purl.uniprot.org/core/date"2016"xsd:gYear
http://purl.uniprot.org/citations/26967533http://purl.uniprot.org/core/name"J Innate Immun"xsd:string
http://purl.uniprot.org/citations/26967533http://purl.uniprot.org/core/pages"284-298"xsd:string
http://purl.uniprot.org/citations/26967533http://purl.uniprot.org/core/title"Staphylococcus aureus Induces Shedding of IL-1RII in Monocytes and Neutrophils."xsd:string
http://purl.uniprot.org/citations/26967533http://purl.uniprot.org/core/volume"8"xsd:string
http://purl.uniprot.org/citations/26967533http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/26967533
http://purl.uniprot.org/citations/26967533http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/26967533
http://purl.uniprot.org/uniprot/#_P27931-mappedCitation-26967533http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/26967533
http://purl.uniprot.org/uniprot/#_Q4FK69-mappedCitation-26967533http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/26967533
http://purl.uniprot.org/uniprot/#_Q8K084-mappedCitation-26967533http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/26967533
http://purl.uniprot.org/uniprot/P27931http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/26967533
http://purl.uniprot.org/uniprot/Q4FK69http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/26967533
http://purl.uniprot.org/uniprot/Q8K084http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/26967533