| http://purl.uniprot.org/citations/9847016 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/9847016 | http://www.w3.org/2000/01/rdf-schema#comment | "To investigate the ability of recombinant human interleukin 10 (rhuIL-10) to suppress the release of inflammatory mediators from lipopolysaccharide (LPS)-stimulated equine macrophages, rhuIL-10 was added to equine peritoneal macrophage monolayers at concentrations of 0, 0.1, 1, 10, or 100 ng/ml. Thirty minutes later, LPS (E. coli O55:B5) was added at final concentrations of 0, 1, 10, 100 ng/ml. Macrophages were incubated for 16 h at 37 degrees C, then supernates were harvested and assayed for tumor necrosis factor (TNF) activity (L929 cytotoxicity), interleukin-6 (IL-6) activity (B9 proliferation), prostaglandin E2 concentration (ELISA), and nitric oxide (Griess reaction for nitrite). Preincubation of LPS-stimulated peritoneal macrophages with rhuIL-10 caused significant (P<0.05) reduction in secretion of TNF, IL-6, and PGE2, in a dose-dependent manner. Of the inflammatory mediators, TNF was most sensitive to the effects of rhuIL-10. At concentrations of rhuIL-10> or =1 ng/ml, TNF activity in the supernate was inhibited significantly at all concentrations of LPS. At one or more LPS concentrations, there was significant inhibition of each mediator in the presence of 1 ng rhuIL-10/ml and, at 100 ng/ml, rhuIL-10 significantly inhibited production of each mediator at all LPS concentrations tested. When data were expressed as a percentage of control values and pooled across all LPS concentrations, both PGE2 and TNF values were significantly reduced at rhuIL-10 concentrations of > or =1 ng/ml, whereas IL-6 was inhibited significantly at concentrations of > or =10 ng rhuIL-10/ml. Tumor necrosis factor production was more completely suppressed (7.8% of control) by the highest concentration of rhuIL-10(100 ng/ml) than was PGE2 (27.2%) or IL-6 (43.8%). Nitrite was not detected in any supernate from peritoneal macrophage monolayers."xsd:string |
| http://purl.uniprot.org/citations/9847016 | http://purl.org/dc/terms/identifier | "doi:10.1016/s0165-2427(98)00181-0"xsd:string |
| http://purl.uniprot.org/citations/9847016 | http://purl.uniprot.org/core/author | "Moldawer L.L."xsd:string |
| http://purl.uniprot.org/citations/9847016 | http://purl.uniprot.org/core/author | "Hawkins D.L."xsd:string |
| http://purl.uniprot.org/citations/9847016 | http://purl.uniprot.org/core/author | "MacKay R.J."xsd:string |
| http://purl.uniprot.org/citations/9847016 | http://purl.uniprot.org/core/author | "MacKay S.L."xsd:string |
| http://purl.uniprot.org/citations/9847016 | http://purl.uniprot.org/core/date | "1998"xsd:gYear |
| http://purl.uniprot.org/citations/9847016 | http://purl.uniprot.org/core/name | "Vet Immunol Immunopathol"xsd:string |
| http://purl.uniprot.org/citations/9847016 | http://purl.uniprot.org/core/pages | "1-10"xsd:string |
| http://purl.uniprot.org/citations/9847016 | http://purl.uniprot.org/core/title | "Human interleukin 10 suppresses production of inflammatory mediators by LPS-stimulated equine peritoneal macrophages."xsd:string |
| http://purl.uniprot.org/citations/9847016 | http://purl.uniprot.org/core/volume | "66"xsd:string |
| http://purl.uniprot.org/citations/9847016 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/9847016 |
| http://purl.uniprot.org/citations/9847016 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/9847016 |
| http://purl.uniprot.org/uniprot/P22301#attribution-76C0398E65C4EFEC806A28CDB3500645 | http://purl.uniprot.org/core/source | http://purl.uniprot.org/citations/9847016 |