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Neutrophils Facilitate Prolonged Inflammasome Response in the DAMP-Rich Inflammatory Milieu

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dc.date.accessioned2021-11-19T01:41:30Z-
dc.date.available2021-11-19T01:41:30Z-
dc.date.issued2021-09-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/185982-
dc.description.abstractAberrant 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.statementOfResponsibilityopen-
dc.languageEnglish-
dc.publisherFrontiers Research Foundation-
dc.relation.isPartOfFRONTIERS IN IMMUNOLOGY-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.titleNeutrophils Facilitate Prolonged Inflammasome Response in the DAMP-Rich Inflammatory Milieu-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentOthers-
dc.contributor.googleauthorSeunghwan Son-
dc.contributor.googleauthorSung-Hyun Yoon-
dc.contributor.googleauthorByeong Jun Chae-
dc.contributor.googleauthorInhwa Hwang-
dc.contributor.googleauthorDo-Wan Shim-
dc.contributor.googleauthorYoung Ho Choe-
dc.contributor.googleauthorYoung-Min Hyun-
dc.contributor.googleauthorJe-Wook Yu-
dc.identifier.doi10.3389/fimmu.2021.746032-
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dc.relation.journalcodeJ03075-
dc.identifier.eissn1664-3224-
dc.identifier.pmid34659244-
dc.subject.keywordDAMP-
dc.subject.keywordNLRP3 desensitization-
dc.subject.keywordSARM1-
dc.subject.keywordefferocytosis-
dc.subject.keywordinflammasome-
dc.subject.keywordneutrophil-
dc.subject.keywordpyroptosis-
dc.contributor.alternativeNameShim, Do-Wan-
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dc.citation.volume12-
dc.citation.startPage746032-
dc.identifier.bibliographicCitationFRONTIERS IN IMMUNOLOGY, Vol.12 : 746032, 2021-09-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Anatomy (해부학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Microbiology (미생물학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Others (기타) > 1. Journal Papers

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