Negative regulation of interleukin 1 beta expression in response to DnaK from Pseudomonas aeruginosa via the PI3K/PDK1/FoxO1 pathways
DC Field | Value | Language |
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dc.contributor.author | Lee, Jung-Hoon | - |
dc.contributor.author | Jeon, Jisu | - |
dc.contributor.author | Bai, Fang | - |
dc.contributor.author | Wu, Weihui | - |
dc.contributor.author | Ha, Un-Hwan | - |
dc.date.accessioned | 2021-08-30T06:35:49Z | - |
dc.date.available | 2021-08-30T06:35:49Z | - |
dc.date.created | 2021-06-19 | - |
dc.date.issued | 2020-12 | - |
dc.identifier.issn | 0147-9571 | - |
dc.identifier.uri | https://scholar.korea.ac.kr/handle/2021.sw.korea/51212 | - |
dc.description.abstract | Interleukin (IL)-1 beta is crucial for a wide range of inflammatory responses. Previously, we reported that IL-1 beta is produced in response to Pseudomonas aeruginosa-derived DnaK via NF-kappa B and JNK pathways; however, the signaling pathways that counter the process to maintain IL-1 beta homeostasis are unknown. Here, we show that DnaK-mediated expression of IL1 beta is increased markedly in macrophages upon blockade of PI3K/PDK1. This was verified by measuring released IL-1 beta protein. The negative effect of PI3K on IL-1 beta production was dependent on suppression of both NF-kappa B and JNK activation. Intriguingly, PDK1 (an underlying mediator of PI3K) acted as an upstream regulator for the activation of NF-kappa B, but downregulated JNK activation. Furthermore, production of IL-1 beta and activation of JNK were triggered by inhibition of phosphorylated FoxO1; phosphorylation of FoxO1 was controlled by PDK1 signaling in response to DnaK. Thus, IL-1 beta production is modulated by P. aeruginosaderived DnaK via cross-talk between JNK and PI3K/PDK1/FoxO1 pathways. | - |
dc.language | English | - |
dc.language.iso | en | - |
dc.publisher | ELSEVIER SCI LTD | - |
dc.subject | HEAT-SHOCK PROTEINS | - |
dc.subject | EXTRACELLULAR HSP70 | - |
dc.subject | ACTIVATION | - |
dc.subject | INFECTION | - |
dc.subject | CYTOKINE | - |
dc.subject | CELLS | - |
dc.subject | LUNG | - |
dc.subject | PHOSPHORYLATION | - |
dc.subject | TRANSCRIPTION | - |
dc.subject | INFLAMMASOME | - |
dc.title | Negative regulation of interleukin 1 beta expression in response to DnaK from Pseudomonas aeruginosa via the PI3K/PDK1/FoxO1 pathways | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Ha, Un-Hwan | - |
dc.identifier.doi | 10.1016/j.cimid.2020.101543 | - |
dc.identifier.scopusid | 2-s2.0-85090701424 | - |
dc.identifier.wosid | 000594775100033 | - |
dc.identifier.bibliographicCitation | COMPARATIVE IMMUNOLOGY MICROBIOLOGY AND INFECTIOUS DISEASES, v.73 | - |
dc.relation.isPartOf | COMPARATIVE IMMUNOLOGY MICROBIOLOGY AND INFECTIOUS DISEASES | - |
dc.citation.title | COMPARATIVE IMMUNOLOGY MICROBIOLOGY AND INFECTIOUS DISEASES | - |
dc.citation.volume | 73 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Immunology | - |
dc.relation.journalResearchArea | Microbiology | - |
dc.relation.journalResearchArea | Veterinary Sciences | - |
dc.relation.journalWebOfScienceCategory | Immunology | - |
dc.relation.journalWebOfScienceCategory | Microbiology | - |
dc.relation.journalWebOfScienceCategory | Veterinary Sciences | - |
dc.subject.keywordPlus | HEAT-SHOCK PROTEINS | - |
dc.subject.keywordPlus | EXTRACELLULAR HSP70 | - |
dc.subject.keywordPlus | ACTIVATION | - |
dc.subject.keywordPlus | INFECTION | - |
dc.subject.keywordPlus | CYTOKINE | - |
dc.subject.keywordPlus | CELLS | - |
dc.subject.keywordPlus | LUNG | - |
dc.subject.keywordPlus | PHOSPHORYLATION | - |
dc.subject.keywordPlus | TRANSCRIPTION | - |
dc.subject.keywordPlus | INFLAMMASOME | - |
dc.subject.keywordAuthor | DnaK | - |
dc.subject.keywordAuthor | FoxO1 | - |
dc.subject.keywordAuthor | IL-1 beta | - |
dc.subject.keywordAuthor | PDK1 | - |
dc.subject.keywordAuthor | PI3K | - |
dc.subject.keywordAuthor | Pseudomonas aeruginosa | - |
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