Bacterial Outer Membrane Vesicle-Mediated Cytosolic Delivery of Flagellin Triggers Host NLRC4 Canonical Inflammasome Signaling
DC Field | Value | Language |
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dc.contributor.author | Yang, Jungmin | - |
dc.contributor.author | Hwang, Inhwa | - |
dc.contributor.author | Lee, Eunju | - |
dc.contributor.author | Shin, Sung Jae | - |
dc.contributor.author | Lee, Eun-Jin | - |
dc.contributor.author | Rhee, Joon Haeng | - |
dc.contributor.author | Yu, Je-Wook | - |
dc.date.accessioned | 2021-08-30T08:21:14Z | - |
dc.date.available | 2021-08-30T08:21:14Z | - |
dc.date.created | 2021-06-18 | - |
dc.date.issued | 2020-11-18 | - |
dc.identifier.issn | 1664-3224 | - |
dc.identifier.uri | https://scholar.korea.ac.kr/handle/2021.sw.korea/51484 | - |
dc.description.abstract | Bacteria-released components can modulate host innate immune response in the absence of direct host cell-bacteria interaction. In particular, bacteria-derived outer membrane vesicles (OMVs) were recently shown to activate host caspase-11-mediated non-canonical inflammasome pathway via deliverance of OMV-bound lipopolysaccharide. However, further precise understanding of innate immune-modulation by bacterial OMVs remains elusive. Here, we present evidence that flagellated bacteria-released OMVs can trigger NLRC4 canonical inflammasome activation via flagellin delivery to the cytoplasm of host cells. Salmonella typhimurium-derived OMVs caused a robust NLRC4-mediated caspase-1 activation and interleukin-1 beta secretion in macrophages in an endocytosis-dependent, but guanylate-binding protein-independent manner. Notably, OMV-associated flagellin is crucial for Salmonella OMV-induced inflammasome response. Flagellated Pseudomonas aeruginosa-released OMVs consistently promoted robust NLRC4 inflammasome activation, while non-flagellated Escherichia coli-released OMVs induced NLRC4-independent non-canonical inflammasome activation leading to NLRP3-mediated interleukin-1 beta secretion. Flagellin-deficient Salmonella OMVs caused a weak interleukin-1 beta production in a NLRP3-dependent manner. These findings indicate that Salmonella OMV triggers NLRC4 inflammasome activation via OMV-associated flagellin in addition to a mild induction of non-canonical inflammasome signaling via OMV-bound lipopolysaccharide. Intriguingly, flagellated Salmonella-derived OMVs induced more rapid inflammasome response than flagellin-deficient Salmonella OMV and non-flagellated Escherichia coli-derived OMVs. Supporting these in vitro results, Nlrc4-deficient mice showed significantly reduced interleukin-1 beta production after intraperitoneal challenge with Salmonella-released OMVs. Taken together, our results here propose that NLRC4 inflammasome machinery is a rapid sensor of bacterial OMV-bound flagellin as a host defense mechanism against bacterial pathogen infection. | - |
dc.language | English | - |
dc.language.iso | en | - |
dc.publisher | FRONTIERS MEDIA SA | - |
dc.subject | AIM2 INFLAMMASOME | - |
dc.subject | ACTIVATION | - |
dc.subject | RECOGNITION | - |
dc.subject | LPS | - |
dc.subject | BIOGENESIS | - |
dc.subject | CASPASE-1 | - |
dc.subject | IL-1-BETA | - |
dc.subject | RECEPTORS | - |
dc.subject | IMMUNITY | - |
dc.title | Bacterial Outer Membrane Vesicle-Mediated Cytosolic Delivery of Flagellin Triggers Host NLRC4 Canonical Inflammasome Signaling | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Lee, Eun-Jin | - |
dc.identifier.doi | 10.3389/fimmu.2020.581165 | - |
dc.identifier.scopusid | 2-s2.0-85097159545 | - |
dc.identifier.wosid | 000594752800001 | - |
dc.identifier.bibliographicCitation | FRONTIERS IN IMMUNOLOGY, v.11 | - |
dc.relation.isPartOf | FRONTIERS IN IMMUNOLOGY | - |
dc.citation.title | FRONTIERS IN IMMUNOLOGY | - |
dc.citation.volume | 11 | - |
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.journalWebOfScienceCategory | Immunology | - |
dc.subject.keywordPlus | AIM2 INFLAMMASOME | - |
dc.subject.keywordPlus | ACTIVATION | - |
dc.subject.keywordPlus | RECOGNITION | - |
dc.subject.keywordPlus | LPS | - |
dc.subject.keywordPlus | BIOGENESIS | - |
dc.subject.keywordPlus | CASPASE-1 | - |
dc.subject.keywordPlus | IL-1-BETA | - |
dc.subject.keywordPlus | RECEPTORS | - |
dc.subject.keywordPlus | IMMUNITY | - |
dc.subject.keywordAuthor | outer membrane vesicles | - |
dc.subject.keywordAuthor | NLRC4 | - |
dc.subject.keywordAuthor | inflammasome | - |
dc.subject.keywordAuthor | interleukin-1 | - |
dc.subject.keywordAuthor | caspase-1 | - |
dc.subject.keywordAuthor | flagellin | - |
dc.subject.keywordAuthor | host defense | - |
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