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Interleukin-1 promotes coagulation, which is necessary for protective immunity in the lung against streptococcus pneumoniae infection
DC Field | Value | Language |
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dc.contributor.author | Yang, Hyungjun | - |
dc.contributor.author | Ko, Hyun-Jeong | - |
dc.contributor.author | Yang, Jin-Young | - |
dc.contributor.author | Kim, Jae-Jin | - |
dc.contributor.author | Seo, Sang-Uk | - |
dc.contributor.author | Park, Seung Gu | - |
dc.contributor.author | Choi, Sun Shim | - |
dc.contributor.author | Seong, Je Kyung | - |
dc.contributor.author | Kweon, Mi-Na | - |
dc.date.accessioned | 2024-08-08T01:44:21Z | - |
dc.date.available | 2024-08-08T01:44:21Z | - |
dc.date.created | 2020-07-10 | - |
dc.date.created | 2020-07-10 | - |
dc.date.issued | 2013-01 | - |
dc.identifier.citation | Journal of Infectious Diseases, Vol.207 No.1, pp.50-60 | - |
dc.identifier.issn | 0022-1899 | - |
dc.identifier.uri | https://hdl.handle.net/10371/207718 | - |
dc.description.abstract | Interleukin (IL)-1 is a well-known cytokine for the initiation of innate immunity in bacterial infection. However, the underlying mechanism of IL-1 on the respiratory infection is not fully elucidated. We studied how IL-1 contributes to the host defense against Streptococcus pneumoniae. IL-1R(-/-) mice showed high mortality, local cytokine storm, and substantial infiltrates in the lower respiratory tract after intratracheal challenge with S. pneumoniae. The IL-1-deficient condition did not suppress the propagation of bacteria in the lung, although the recruitment and the bacteria-killing ability of neutrophils (CD11b(+)Ly6C(+)Ly6G(+)) were not defective compared with wild-type mice. Unexpectedly, we found that the transcription of fibrinogen alpha and gamma genes were highly activated in the lungs of wild-type mice after the infection, whereas no significant changes were found in IL-1R(-/-) mice. Of note, synthesis of fibrinogen was dependent on the IL-1-IL-6-Stat3 cascade. Treatment with recombinant fibrinogen improved survival and bacterial propagation in the IL-1R(-/-) mice and blockade of the coagulation increased the susceptibility of wild-type mice to pneumococcal pneumonia. Our findings suggest that IL-1 signaling leads to the synthesis of fibrinogen in the lung after pneumococcus infection and is followed by coagulation, which contributes to the control of bacterial infection in the pulmonary tract. | - |
dc.language | 영어 | - |
dc.publisher | University of Chicago Press | - |
dc.title | Interleukin-1 promotes coagulation, which is necessary for protective immunity in the lung against streptococcus pneumoniae infection | - |
dc.type | Article | - |
dc.identifier.doi | 10.1093/infdis/jis651 | - |
dc.citation.journaltitle | Journal of Infectious Diseases | - |
dc.identifier.wosid | 000312604200008 | - |
dc.identifier.scopusid | 2-s2.0-84872967043 | - |
dc.citation.endpage | 60 | - |
dc.citation.number | 1 | - |
dc.citation.startpage | 50 | - |
dc.citation.volume | 207 | - |
dc.description.isOpenAccess | Y | - |
dc.contributor.affiliatedAuthor | Seong, Je Kyung | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.subject.keywordPlus | GAMMA-FIBRINOGEN PROMOTER | - |
dc.subject.keywordPlus | IMPAIRED HOST-DEFENSE | - |
dc.subject.keywordPlus | GENE-EXPRESSION | - |
dc.subject.keywordPlus | INNATE IMMUNITY | - |
dc.subject.keywordPlus | DEFICIENT MICE | - |
dc.subject.keywordPlus | I RECEPTOR | - |
dc.subject.keywordPlus | ACTIVATION | - |
dc.subject.keywordPlus | IL-1 | - |
dc.subject.keywordPlus | INDUCTION | - |
dc.subject.keywordPlus | APOPTOSIS | - |
dc.subject.keywordAuthor | IL-1 | - |
dc.subject.keywordAuthor | S. pneumoniae | - |
dc.subject.keywordAuthor | coagulation | - |
dc.subject.keywordAuthor | fibrinogen | - |
dc.subject.keywordAuthor | innate immunity | - |
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