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Neutrophils Facilitate Prolonged Inflammasome Response in the DAMP-Rich Inflammatory Milieu
DC Field | Value | Language |
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dc.contributor.author | 심도완 | - |
dc.contributor.author | 유제욱 | - |
dc.contributor.author | 현영민 | - |
dc.contributor.author | 황인화 | - |
dc.date.accessioned | 2021-11-19T01:41:30Z | - |
dc.date.available | 2021-11-19T01:41:30Z | - |
dc.date.issued | 2021-09 | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/185982 | - |
dc.description.abstract | Aberrant inflammasome activation contributes to various chronic inflammatory diseases; however, pyroptosis of inflammasome-active cells promptly terminates local inflammasome response. Molecular mechanisms underlying prolonged inflammasome signaling thus require further elucidation. Here, we report that neutrophil-specific resistance to pyroptosis and NLRP3 desensitization can facilitate sustained inflammasome response and interleukin-1β secretion. Unlike macrophages, inflammasome-activated neutrophils did not undergo pyroptosis, indicated by using in vitro cell-based assay and in vivo mouse model. Intriguingly, danger-associated molecular patterns (DAMP)-rich milieu in the inflammatory region significantly abrogated NLRP3-activating potential of macrophages, but not of neutrophils. This macrophage-specific NLRP3 desensitization was associated with DAMP-induced mitochondrial depolarization that was not observed in neutrophils due to a lack of SARM1 expression. Indeed, valinomycin-induced compulsory mitochondrial depolarization in neutrophils restored inflammasome-dependent cell death and ATP-induced NLRP3 desensitization in neutrophils. Alongside prolonged inflammasome-activating potential, neutrophils predominantly secreted interleukin-1β rather than other proinflammatory cytokines upon NLRP3 stimulation. Furthermore, inflammasome-activated neutrophils did not trigger efferocytosis-mediated M2 macrophage polarization essential for the initiation of inflammation resolution. Taken together, our results indicate that neutrophils can prolong inflammasome response via mitochondria-dependent resistance to NLRP3 desensitization and function as major interleukin-1β-secreting cells in DAMP-rich inflammatory region. | - |
dc.description.statementOfResponsibility | open | - |
dc.format | application/pdf | - |
dc.language | English | - |
dc.publisher | Frontiers Research Foundation | - |
dc.relation.isPartOf | FRONTIERS IN IMMUNOLOGY | - |
dc.rights | CC BY-NC-ND 2.0 KR | - |
dc.title | Neutrophils Facilitate Prolonged Inflammasome Response in the DAMP-Rich Inflammatory Milieu | - |
dc.type | Article | - |
dc.contributor.college | College of Medicine (의과대학) | - |
dc.contributor.department | Others | - |
dc.contributor.googleauthor | Seunghwan Son | - |
dc.contributor.googleauthor | Sung-Hyun Yoon | - |
dc.contributor.googleauthor | Byeong Jun Chae | - |
dc.contributor.googleauthor | Inhwa Hwang | - |
dc.contributor.googleauthor | Do-Wan Shim | - |
dc.contributor.googleauthor | Young Ho Choe | - |
dc.contributor.googleauthor | Young-Min Hyun | - |
dc.contributor.googleauthor | Je-Wook Yu | - |
dc.identifier.doi | 10.3389/fimmu.2021.746032 | - |
dc.contributor.localId | A06149 | - |
dc.contributor.localId | A02508 | - |
dc.contributor.localId | A04814 | - |
dc.contributor.localId | A05445 | - |
dc.relation.journalcode | J03075 | - |
dc.identifier.eissn | 1664-3224 | - |
dc.identifier.pmid | 34659244 | - |
dc.subject.keyword | DAMP | - |
dc.subject.keyword | NLRP3 desensitization | - |
dc.subject.keyword | SARM1 | - |
dc.subject.keyword | efferocytosis | - |
dc.subject.keyword | inflammasome | - |
dc.subject.keyword | neutrophil | - |
dc.subject.keyword | pyroptosis | - |
dc.contributor.alternativeName | Shim, Do-Wan | - |
dc.contributor.affiliatedAuthor | 심도완 | - |
dc.contributor.affiliatedAuthor | 유제욱 | - |
dc.contributor.affiliatedAuthor | 현영민 | - |
dc.contributor.affiliatedAuthor | 황인화 | - |
dc.citation.volume | 12 | - |
dc.citation.startPage | 746032 | - |
dc.identifier.bibliographicCitation | FRONTIERS IN IMMUNOLOGY, Vol.12 : 746032, 2021-09 | - |
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