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dc.contributor.authorPeres, Raphael Sanches
dc.contributor.authorChiuso-Minicucci, Fernanda
dc.contributor.authorda Rosa, Larissa Camargo
dc.contributor.authorDomingues, Alexandre [UNESP]
dc.contributor.authorZorzella-Pezavento, Sofia Fernanda Gonçalves
dc.contributor.authorFrança, Thais Graziela Donegá
dc.contributor.authorIshikawa, Larissa Lumi Watanabe
dc.contributor.authordo Amarante, Alessandro Francisco Talamini [UNESP]
dc.contributor.authorSartori, Alexandrina [UNESP]
dc.date.accessioned2014-05-27T11:29:34Z
dc.date.available2014-05-27T11:29:34Z
dc.date.issued2013-06-01
dc.identifierhttp://dx.doi.org/10.1016/j.exppara.2013.03.007
dc.identifier.citationExperimental Parasitology, v. 134, n. 2, p. 183-189, 2013.
dc.identifier.issn0014-4894
dc.identifier.issn1090-2449
dc.identifier.urihttp://hdl.handle.net/11449/75512
dc.description.abstractEpidemiological and experimental studies support the idea that helminth infections can induce a protective effect against the development of autoimmune and allergic diseases. In this study we characterized the immune response induced by Strongyloides venezuelensis infection in C57BL/6 mice and then evaluated the effect of a previous contact with this helminth in the outcome of type 1 diabetes. Animals were initially infected with 2000 L3 larvae from S. venezuelensis and euthanized 22. days later. An acute phase, identified by a high amount of eggs per gram of feces, was established between days 7 and 9 post-infection. Recovery from infection was associated with a Th2 polarized response characterized by a significant level of serum IgG1 specific antibodies and also a significant production of IL-5 and IL-10 by spleen cells stimulated with S. venezuelensis soluble antigen. Immunization with soluble S. venezuelensis antigen associated with complete Freund's adjuvant followed by infection with S. venezuelensis protected mice from diabetes development induced by streptozotocin. Protection was characterized by a higher body weight gain, lower glycemic levels, much less severe insulitis and preserved insulin production. Together, these results indicate that S. venezuelensis contributed to protect C57BL/6 mice against experimental diabetes induced by streptozotocin. © 2013 Elsevier Inc.en
dc.format.extent183-189
dc.language.isoeng
dc.relation.ispartofExperimental Parasitology
dc.sourceScopus
dc.subjectExperimental diabetes
dc.subjectHygiene hypothesis
dc.subjectS. venezuelensis
dc.subjectStreptozotocin
dc.subjectFreund adjuvant
dc.subjectgamma interferon
dc.subjectimmunoglobulin G1
dc.subjectinsulin
dc.subjectinterleukin 10
dc.subjectinterleukin 5
dc.subjectparasite antigen
dc.subjectStrongyloides venezuelensis antigen
dc.subjectunclassified drug
dc.subjectanimal experiment
dc.subjectanimal model
dc.subjectanimal tissue
dc.subjectbody weight
dc.subjectcontrolled study
dc.subjectcytokine production
dc.subjectdrug efficacy
dc.subjectimmune response
dc.subjectimmunization
dc.subjectimmunoglobulin blood level
dc.subjectimmunomodulation
dc.subjectinsulin dependent diabetes mellitus
dc.subjectinsulitis
dc.subjectmale
dc.subjectmouse
dc.subjectnonhuman
dc.subjectpriority journal
dc.subjectspleen cell
dc.subjectStrongyloides venezuelensis
dc.subjectstrongyloidiasis
dc.subjecttreatment response
dc.subjectweight reduction
dc.subjectAnimals
dc.subjectAntibodies, Helminth
dc.subjectBlood Glucose
dc.subjectCytokines
dc.subjectDiabetes Mellitus, Experimental
dc.subjectDiabetes Mellitus, Type 1
dc.subjectFeces
dc.subjectInsulin
dc.subjectIslets of Langerhans
dc.subjectMale
dc.subjectMice
dc.subjectMice, Inbred C57BL
dc.subjectParasite Egg Count
dc.subjectRats
dc.subjectRats, Wistar
dc.subjectSpleen
dc.subjectStreptozocin
dc.subjectStrongyloides
dc.subjectStrongyloidiasis
dc.subjectTh2 Cells
dc.titlePrevious contact with Strongyloides venezuelensis contributed to prevent insulitis in MLD-STZ diabetesen
dc.typeArtigo
dcterms.licensehttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dc.contributor.institutionUniversidade Estadual Paulista (UNESP)
dc.description.affiliationDepartment of Microbiology and Immunology Biosciences Institute, Univ Estadual Paulista (UNESP), Botucatu, São Paulo
dc.description.affiliationDepartment of Pathology Botucatu Medical School Univ Estadual Paulista (UNESP), Botucatu, São Paulo
dc.description.affiliationDepartment of Parasitology Biosciences Institute Univ Estadual Paulista (UNESP), Botucatu, São Paulo
dc.description.affiliationUnespDepartment of Pathology Botucatu Medical School Univ Estadual Paulista (UNESP), Botucatu, São Paulo
dc.description.affiliationUnespDepartment of Parasitology Biosciences Institute Univ Estadual Paulista (UNESP), Botucatu, São Paulo
dc.identifier.doi10.1016/j.exppara.2013.03.007
dc.identifier.wosWOS:000319542800010
dc.rights.accessRightsAcesso aberto
dc.identifier.scopus2-s2.0-84876318616
unesp.campusUniversidade Estadual Paulista (UNESP), Instituto de Biociências, Botucatupt
unesp.campusUniversidade Estadual Paulista (UNESP), Faculdade de Medicina, Botucatupt
dc.identifier.file2-s2.0-84876318616.pdf
dc.identifier.lattes4977572416129527
dc.identifier.lattes2677231663329706
unesp.author.lattes4977572416129527
unesp.author.lattes2677231663329706
unesp.author.orcid0000-0003-4557-3331[9]
unesp.author.orcid0000-0003-3481-2181[7]
unesp.author.orcid0000-0003-3995-5501[8]
unesp.author.orcid0000-0001-9030-0768[5]
unesp.author.orcid0000-0002-0417-779X[1]
dc.relation.ispartofjcr1.821
dc.relation.ispartofsjr0,635
dc.relation.ispartofsjr0,635
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