Protective effect of C-reactive protein against the lethality induced by Vibrio vulnificus lipopolysaccharide

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dc.contributor.authorChae, MRko
dc.contributor.authorPark, BHko
dc.contributor.authorKim, JSko
dc.contributor.authorRho, HWko
dc.contributor.authorPark, JWko
dc.contributor.authorKim, HRko
dc.date.accessioned2024-03-22T06:04:25Z-
dc.date.available2024-03-22T06:04:25Z-
dc.date.created2024-03-21-
dc.date.created2024-03-21-
dc.date.issued2000-
dc.identifier.citationMICROBIOLOGY AND IMMUNOLOGY, v.44, no.5, pp.335 - 340-
dc.identifier.issn0385-5600-
dc.identifier.urihttp://hdl.handle.net/10203/318767-
dc.description.abstractVibrio vulnificus infection has attracted special interest because of its high mortality. A strong clinical association exists between hepatic dysfunction and increased morbidity and mortality from V. vulnificus infection. In this study, the effect of C-reactive protein (CRP), a typical hepatogenic acute phase protein, on the lethality induced by V. vulnificus lipopolysaccharide (LPS) was investigated in galactosamine-sensitized mice. The pretreatment of CRP, in a dose of at least 2 mg/kg, 2 hr before the challenge of LPS completely protected mice against the lethality by V. vulnificus LPS, The elevation of serum tumor necrosis factor-alpha (TNF-alpha) induced by LPS administration was not affected by CRP pretreatment, However, the LPS- or TNF-alpha-induced hepatotoxicity was completely prevented by CRP, These results indicate that CRP does not prevent the synthesis, but prevents the hepatotoxic action of TNF-alpha. The possibility that impaired production of acute phase proteins in patients with pre-existing hepatic dysfunction may predispose the higher risk of V. vulnificus infection needs to be evaluated further.-
dc.languageEnglish-
dc.publisherCENTER ACADEMIC PUBL JAPAN-
dc.titleProtective effect of C-reactive protein against the lethality induced by Vibrio vulnificus lipopolysaccharide-
dc.typeArticle-
dc.identifier.wosid000086971700001-
dc.identifier.scopusid2-s2.0-0034044587-
dc.type.rimsART-
dc.citation.volume44-
dc.citation.issue5-
dc.citation.beginningpage335-
dc.citation.endingpage340-
dc.citation.publicationnameMICROBIOLOGY AND IMMUNOLOGY-
dc.identifier.doi10.1111/j.1348-0421.2000.tb02503.x-
dc.contributor.localauthorPark, BH-
dc.contributor.nonIdAuthorChae, MR-
dc.contributor.nonIdAuthorKim, JS-
dc.contributor.nonIdAuthorRho, HW-
dc.contributor.nonIdAuthorPark, JW-
dc.contributor.nonIdAuthorKim, HR-
dc.description.isOpenAccessN-
dc.type.journalArticleArticle-
dc.subject.keywordAuthorC-reactive protein-
dc.subject.keywordAuthorVibrio vulnificus-
dc.subject.keywordAuthorlipopolysaccharide-
dc.subject.keywordAuthortumor necrosis factor-alpha-
dc.subject.keywordPlusTUMOR-NECROSIS-FACTOR-
dc.subject.keywordPlusGALACTOSAMINE-TREATED MICE-
dc.subject.keywordPlusACUTE-PHASE PROTEINS-
dc.subject.keywordPlusFACTOR-ALPHA-
dc.subject.keywordPlusENDOTOXIN-
dc.subject.keywordPlusPATHOGENESIS-
dc.subject.keywordPlusSERUM-
dc.subject.keywordPlusBLOOD-
dc.subject.keywordPlusINFLAMMATION-
dc.subject.keywordPlusEPIDEMIOLOGY-
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