FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W1968221489> ?p ?o ?g. }

• W1968221489 endingPage "S118" @default.
• W1968221489 startingPage "S118" @default.
• W1968221489 abstract "Background and Aims: Innate immune recognition of microbial components is dependent on pattern recognition receptors (PRRs), which detect components of foreign pathogens referred to as pathogen associated molecular patterns (PAMPs). One important group of PRRs consists of the so called Toll like receptors (TLRs), which activate a network of signal pathways leading to activation of the transcription factors IRF3, NF-uB and AP-1 and subsequent expression of pro-inflammatory cytokines and type I interferons (IFN). Methods: Peripheral blood mononuclear cells (PBMC) were isolated from human blood (healthy volunteers, man) by Ficoll Paque centrifugation. CD14 positive cells were separated by magnetically labelled beads and cultured for 9 days in the presence of M-CSF to differentiate them into macrophages. Thereafter cells were stimulated with different TLR ligands in presence or absence of hydrophobic bile acids like taurolithocholic acid (TLC), glycochenodeoxycholic acid (GCDC) and taurochenodeoxycholic acid (TCDC). Cells were lysed and mRNA and protein expression were measured by realtime PCR and immunoblot respectively. Results: Hydrophobic bile acids changed cytokine expression pattern of TLR ligand stimulated macrophages. LPS-induced TNF-a, IL-6 and IFN-bmRNA expression and expression of antiviral proteins like MxA and PKR were significantly downregulated in response to hydrophobic bile acids, however LPS-induced expression of the strong inhibitory anti-inflammatory interleukin-10 was not modulated. These effects could be mimicked by cAMP. TLC also inhibited TNF-a and IFN-b mRNA expression induced by other TLR ligands like TLR 2, 3, 7 and 9. Phosphorylation of TLR4 dependent signaling elements like p-IRF3 (Ser) and p-p65 (Ser) were not effected by bile acids. However, the inhibitory effect of bile acids on cytokine expression was accompanied by elevation of cAMP and could be reverted by blocking proteinkinase A. This suggested an involvement of the bile acid receptor TGR5 in inhibition of TLR-responses, which we detected in human macrophages by immunostaining. Conclusions: These data show that bile acids mediate immunosuppressive effects by blocking TLR-induced activation of innate immunity responses in human macrophages, thereby probably changing differentiation and activation of macrophages. This may contribute to the known clinical observations that cholestatic patients with high serum bile acid concentrations show reduced cell mediated immunity." @default.
• W1968221489 created "2016-06-24" @default.
• W1968221489 creator A5006774078 @default.
• W1968221489 creator A5015113002 @default.
• W1968221489 creator A5027772237 @default.
• W1968221489 creator A5050181339 @default.
• W1968221489 creator A5062761846 @default.
• W1968221489 creator A5072400601 @default.
• W1968221489 date "2011-03-01" @default.
• W1968221489 modified "2023-10-16" @default.
• W1968221489 title "289 INHIBITION OF TOLL-LIKE RECEPTOR SIGNALING IN HUMAN MACROPHAGES BY BILE ACIDS" @default.
• W1968221489 doi "https://doi.org/10.1016/s0168-8278(11)60291-2" @default.
• W1968221489 hasPublicationYear "2011" @default.
• W1968221489 type Work @default.
• W1968221489 sameAs 1968221489 @default.
• W1968221489 citedByCount "0" @default.
• W1968221489 crossrefType "journal-article" @default.
• W1968221489 hasAuthorship W1968221489A5006774078 @default.
• W1968221489 hasAuthorship W1968221489A5015113002 @default.
• W1968221489 hasAuthorship W1968221489A5027772237 @default.
• W1968221489 hasAuthorship W1968221489A5050181339 @default.
• W1968221489 hasAuthorship W1968221489A5062761846 @default.
• W1968221489 hasAuthorship W1968221489A5072400601 @default.
• W1968221489 hasConcept C136449434 @default.
• W1968221489 hasConcept C170493617 @default.
• W1968221489 hasConcept C185592680 @default.
• W1968221489 hasConcept C203014093 @default.
• W1968221489 hasConcept C2776709828 @default.
• W1968221489 hasConcept C2778025104 @default.
• W1968221489 hasConcept C55493867 @default.
• W1968221489 hasConcept C86803240 @default.
• W1968221489 hasConcept C95444343 @default.
• W1968221489 hasConceptScore W1968221489C136449434 @default.
• W1968221489 hasConceptScore W1968221489C170493617 @default.
• W1968221489 hasConceptScore W1968221489C185592680 @default.
• W1968221489 hasConceptScore W1968221489C203014093 @default.
• W1968221489 hasConceptScore W1968221489C2776709828 @default.
• W1968221489 hasConceptScore W1968221489C2778025104 @default.
• W1968221489 hasConceptScore W1968221489C55493867 @default.
• W1968221489 hasConceptScore W1968221489C86803240 @default.
• W1968221489 hasConceptScore W1968221489C95444343 @default.
• W1968221489 hasLocation W19682214891 @default.
• W1968221489 hasOpenAccess W1968221489 @default.
• W1968221489 hasPrimaryLocation W19682214891 @default.
• W1968221489 hasRelatedWork W1967636949 @default.
• W1968221489 hasRelatedWork W1982297066 @default.
• W1968221489 hasRelatedWork W1987584618 @default.
• W1968221489 hasRelatedWork W2032137356 @default.
• W1968221489 hasRelatedWork W2041645124 @default.
• W1968221489 hasRelatedWork W2347913873 @default.
• W1968221489 hasRelatedWork W2366655330 @default.
• W1968221489 hasRelatedWork W2371450007 @default.
• W1968221489 hasRelatedWork W3149127145 @default.
• W1968221489 hasRelatedWork W3161574264 @default.
• W1968221489 hasVolume "54" @default.
• W1968221489 isParatext "false" @default.
• W1968221489 isRetracted "false" @default.
• W1968221489 magId "1968221489" @default.
• W1968221489 workType "article" @default.