Unveiling the Crucial Role of Type IV Secretion System and Motility ofHelicobacter pyloriin IL-1 beta Production via NLRP3 Inflammasome Activation in Neutrophils
DC Field | Value | Language |
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dc.contributor.author | Jang, Ah-Ra | - |
dc.contributor.author | Kang, Min-Jung | - |
dc.contributor.author | Shin, Jeong-Ih | - |
dc.contributor.author | Kwon, Soon-Wook | - |
dc.contributor.author | Park, Ji-Yeon | - |
dc.contributor.author | Ahn, Jae-Hun | - |
dc.contributor.author | Lee, Tae-Sung | - |
dc.contributor.author | Kim, Dong-Yeon | - |
dc.contributor.author | Choi, Bo-Gwon | - |
dc.contributor.author | Seo, Myoung-Won | - |
dc.contributor.author | Yang, Soo-Jin | - |
dc.contributor.author | Shin, Min-Kyoung | - |
dc.contributor.author | Park, Jong-Hwan | - |
dc.date.accessioned | 2022-01-12T01:42:18Z | - |
dc.date.available | 2022-01-12T01:42:18Z | - |
dc.date.issued | 2020-06 | - |
dc.identifier.issn | 1664-3224 | - |
dc.identifier.issn | 1664-3224 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/53317 | - |
dc.description.abstract | Helicobacter pyloriis a gram-negative, microaerophilic, and spiral-shaped bacterium and causes gastrointestinal diseases in human. IL-1 beta is a representative cytokine produced in innate immune cells and is considered to be a key factor in the development of gastrointestinal malignancies. However, the mechanism of IL-1 beta production by neutrophils duringH. pyloriinfection is still unknown. We designed this study to identify host and bacterial factors involved in regulation ofH. pylori-induced IL-1 beta production in neutrophils. We found thatH. pylori-induced IL-1 beta production is abolished in NLRP3-, ASC-, and caspase-1/11-deficient neutrophils, suggesting essential role for NLRP3 inflammasome in IL-1 beta response againstH. pylori. Host TLR2, but not TLR4 and Nod2, was also required for transcription of NLRP3 and IL-1 beta as well as secretion of IL-1 beta.H. pylorilackingcagL, a key component of the type IV secretion system (T4SS), induced less IL-1 beta production in neutrophils than did its isogenic WT strain, whereasvacAandureAwere dispensable. Moreover, T4SS was involved in caspase-1 activation and IL-1 beta maturation inH. pylori-infected neutrophils. We also found that FlaA is essential forH. pylori-mediated IL-1 beta production in neutrophils, but not dendritic cells. TLR5 and NLRC4 were not required forH. pylori-induced IL-1 beta production in neutrophils. Instead, bacterial motility is essential for the production of IL-1 beta in response toH. pylori. In conclusion, our study shows that host TLR2 and NLRP3 inflammasome and bacterial T4SS and motility are essential factors for IL-1 beta production by neutrophils in response toH. pylori. | - |
dc.language | 영어 | - |
dc.language.iso | ENG | - |
dc.publisher | FRONTIERS MEDIA SA | - |
dc.title | Unveiling the Crucial Role of Type IV Secretion System and Motility ofHelicobacter pyloriin IL-1 beta Production via NLRP3 Inflammasome Activation in Neutrophils | - |
dc.type | Article | - |
dc.identifier.doi | 10.3389/fimmu.2020.01121 | - |
dc.identifier.bibliographicCitation | FRONTIERS IN IMMUNOLOGY, v.11 | - |
dc.description.isOpenAccess | N | - |
dc.identifier.wosid | 000543361900001 | - |
dc.identifier.scopusid | 2-s2.0-85087030459 | - |
dc.citation.title | FRONTIERS IN IMMUNOLOGY | - |
dc.citation.volume | 11 | - |
dc.type.docType | Article | - |
dc.publisher.location | 스위스 | - |
dc.subject.keywordAuthor | bacterial motility | - |
dc.subject.keywordAuthor | Helicobacter pylori | - |
dc.subject.keywordAuthor | IL-1 beta | - |
dc.subject.keywordAuthor | neutrophils | - |
dc.subject.keywordAuthor | type IV secretion system (T4SS) | - |
dc.subject.keywordPlus | HELICOBACTER-PYLORI | - |
dc.subject.keywordPlus | GASTRIC-CANCER | - |
dc.subject.keywordPlus | INCREASED RISK | - |
dc.subject.keywordPlus | BACTERIAL FLAGELLIN | - |
dc.subject.keywordPlus | INTERLEUKIN-1-BETA | - |
dc.subject.keywordPlus | GENE | - |
dc.subject.keywordPlus | POLYMORPHISMS | - |
dc.subject.keywordPlus | EXPRESSION | - |
dc.subject.keywordPlus | INFECTION | - |
dc.subject.keywordPlus | REQUIRES | - |
dc.relation.journalResearchArea | Immunology | - |
dc.relation.journalWebOfScienceCategory | Immunology | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
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