| http://purl.uniprot.org/citations/28835457 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/28835457 | http://www.w3.org/2000/01/rdf-schema#comment | "Heterodimeric IL-27 (p28/EBV-induced gene 3) is an important member of the IL-6/IL-12 cytokine family. IL-27 is predominantly synthesized by mononuclear phagocytes and exerts immunoregulatory functional activities on lymphocytic and nonlymphocytic cells during infection, autoimmunity or neoplasms. There is a great body of evidence on the bidirectional interplay between the autonomic nervous system and immune responses during inflammatory disorders, but so far IL-27 has not been defined as a part of these multifaceted neuroendocrine networks. In this study, we describe the role of catecholamines (as mediators of the sympathetic nervous system) related to IL-27 production in primary mouse macrophages. Noradrenaline and adrenaline dose-dependently suppressed the release of IL-27p28 in LPS/TLR4-activated macrophages, which was independent of α1 adrenoceptors. Instead, β2 adrenoceptor activation was responsible for mediating gene silencing of IL-27p28 and EBV-induced gene 3. The β2 adrenoceptor agonists formoterol and salbutamol mediated suppression of IL-27p28 production, when triggered by zymosan/TLR2, LPS/TLR4, or R848/TLR7/8 activation, but selectively spared the polyinosinic-polycytidylic acid/TLR3 pathway. Mechanistically, β2 adrenergic signaling reinforced an autocrine feedback loop of macrophage-derived IL-10 and this synergized with inhibition of the JNK pathway for limiting IL-27p28. The JNK inhibitors SP600125 and AEG3482 strongly decreased intracellular IL-27p28 in F4/80+CD11b+ macrophages. In endotoxic shock of C57BL/6J mice, pharmacologic activation of β2 adrenoceptors improved the severity of shock, including hypothermia and decreased circulating IL-27p28. Conversely, IL-27p28 was 2.7-fold increased by removal of the catecholamine-producing adrenal glands prior to endotoxic shock. These data suggest a novel role of the sympathetic neuroendocrine system for the modulation of IL-27-dependent acute inflammation."xsd:string |
| http://purl.uniprot.org/citations/28835457 | http://purl.org/dc/terms/identifier | "doi:10.4049/jimmunol.1700687"xsd:string |
| http://purl.uniprot.org/citations/28835457 | http://purl.uniprot.org/core/author | "Radsak M.P."xsd:string |
| http://purl.uniprot.org/citations/28835457 | http://purl.uniprot.org/core/author | "Gericke A."xsd:string |
| http://purl.uniprot.org/citations/28835457 | http://purl.uniprot.org/core/author | "Bosmann M."xsd:string |
| http://purl.uniprot.org/citations/28835457 | http://purl.uniprot.org/core/author | "Roewe J."xsd:string |
| http://purl.uniprot.org/citations/28835457 | http://purl.uniprot.org/core/author | "Riehl D.R."xsd:string |
| http://purl.uniprot.org/citations/28835457 | http://purl.uniprot.org/core/author | "Higer M."xsd:string |
| http://purl.uniprot.org/citations/28835457 | http://purl.uniprot.org/core/date | "2017"xsd:gYear |
| http://purl.uniprot.org/citations/28835457 | http://purl.uniprot.org/core/name | "J Immunol"xsd:string |
| http://purl.uniprot.org/citations/28835457 | http://purl.uniprot.org/core/pages | "2503-2514"xsd:string |
| http://purl.uniprot.org/citations/28835457 | http://purl.uniprot.org/core/title | "Neuroendocrine Modulation of IL-27 in Macrophages."xsd:string |
| http://purl.uniprot.org/citations/28835457 | http://purl.uniprot.org/core/volume | "199"xsd:string |
| http://purl.uniprot.org/citations/28835457 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/28835457 |
| http://purl.uniprot.org/citations/28835457 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/28835457 |
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