Evaluation of the host response to endotoxemia of FVIII and FIX deficient mice

dc.creatorVancine, SMC
dc.creatorPicoli-Quaino, SK
dc.creatorCosta, DSP
dc.creatorMontalvao, SAL
dc.creatorOzelo, MC
dc.creatorAnnichino-Bizzacchi, JM
dc.creatorDe Paula, EV
dc.date2011
dc.dateSEP
dc.date2014-07-30T17:28:17Z
dc.date2015-11-26T16:46:47Z
dc.date2014-07-30T17:28:17Z
dc.date2015-11-26T16:46:47Z
dc.date.accessioned2018-03-28T23:32:43Z
dc.date.available2018-03-28T23:32:43Z
dc.identifierHaemophilia. Wiley-blackwell, v. 17, n. 5, n. 800, n. 807, 2011.
dc.identifier1351-8216
dc.identifierWOS:000294174300046
dc.identifier10.1111/j.1365-2516.2011.02598.x
dc.identifierhttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/65978
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/65978
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1274636
dc.descriptionFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.descriptionConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.descriptionFor several years, coagulation has been implicated in the pathogenesis of sepsis. However, results from clinical trials with natural anticoagulants, as well as studies with knock-out mice for specific coagulation factors yielded conflicting results on the role of coagulation in the pathogenesis of sepsis. The aim of this study was to evaluate the impact of severe The factor VIII: C (FVIII: C) and factor IX: C (FIX: C) deficiency on a lipopolysaccharide (LPS)-induced murine model of sepsis. FVIII: C and FIX: C deficient mice, and their haemostatic normal littermate controls were challenged with LPS, and several parameters of the host response were evaluated: seven-day survival experiments were performed using two dose levels of LPS; biochemical and histological markers of tissue damage, coagulation parameters, and pro-inflammatory cytokines were evaluated at baseline and after 3 h and 6 h after an injection of LPS. Severe FVIII and FIX deficiency were compatible with normal survival in experimental sepsis. In addition, LPS-induced tissue damage and coagulation activation were similar in FVIII or FIX deficient mice compared to their respective controls. A lower release of pro-inflammatory cytokines was observed in FIX but not in FVIII deficient mice. Severe FIX or FVIII deficiency does not protect mice from mortality or from tissue damage in the endotoxemia model, supporting the hypothesis that FVIII and FIX are not critical to the pathogenesis of experimental sepsis.
dc.description17
dc.description5
dc.description800
dc.description807
dc.descriptionFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.descriptionConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.descriptionFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.descriptionConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.descriptionFAPESP [2008/50729-9]
dc.languageen
dc.publisherWiley-blackwell
dc.publisherMalden
dc.publisherEUA
dc.relationHaemophilia
dc.relationHaemophilia
dc.rightsfechado
dc.rightshttp://olabout.wiley.com/WileyCDA/Section/id-406071.html
dc.sourceWeb of Science
dc.subjectdisseminated intravascular coagulation
dc.subjectendotoxemia
dc.subjectfactor IX
dc.subjectfactor VIII
dc.subjecthaemophilia
dc.subjectsepsis
dc.subjectDisseminated Intravascular Coagulation
dc.subjectRandomized Controlled-trial
dc.subjectActivated Protein-c
dc.subjectSevere Sepsis
dc.subjectHemophilia-b
dc.subjectMouse Model
dc.subjectInhibitor
dc.subjectMonocytes
dc.subjectEfficacy
dc.subjectSafety
dc.titleEvaluation of the host response to endotoxemia of FVIII and FIX deficient mice
dc.typeArtículos de revistas


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