Mycobacterium leprae Hsp65 administration reduces the lifespan of aged high antibody producer mice

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dc.contributor.author Baldon, Estevam Jose
dc.contributor.author Marengo, Eliana Blini
dc.contributor.author Franco, Marcelo de
dc.contributor.author Starobinas, Nancy
dc.contributor.author Bueno, Valquiria [UNIFESP]
dc.contributor.author Sant'Anna, Osvaldo Augusto
dc.date.accessioned 2016-01-24T14:35:28Z
dc.date.available 2016-01-24T14:35:28Z
dc.date.issued 2014-03-26
dc.identifier http://dx.doi.org/10.1186/1742-4933-11-6
dc.identifier.citation Immunity & Ageing. London: Biomed Central Ltd, v. 11, 10 p., 2014.
dc.identifier.issn 1742-4933
dc.identifier.uri http://repositorio.unifesp.br/handle/11600/37560
dc.description.abstract Background: Aging process may result in immune modifications that lead to disruption of innate and acquired immunity mechanisms that may induce chronic-degenerative events. the heat shock proteins (Hsp), phylogeneticaly conserved among organisms, present as main function the ability of folding and refolding proteins, but they also are associated with chronic-degenerative disorders. Here were evaluated the role of M. leprae native Hsp65 (WT) and its point-mutated (K(409)A) on survival and anti-DNA and anti-Hsp65 antibody production of aged genetically selected mice for high (H-III) and low (L-III) antibody production; data from 120- and 270-days old mice (named adult or aged, respectively) were compared.Results: WT Hsp65 administration induces reduction in the mean survival time of adult and aged female HIII mice, this effect being stronger in aged individuals. Surprisingly, the native protein administration increased the survival of aged female LIII when compared to K(409)A and control groups. No survival differences were observed in aged male mice after Hsp65 proteins inoculation. We observed increase in IgG1 anti-Hsp65 in WT and K(409)A aged HIII female mice groups and no marked changes in the anti-DNA (adult and aged HIII) and anti-Hsp65 IgG1 or IgG2a isotypes production in adult HIII female and aged male mice. LIII male mice presented increased anti-DNA and anti-Hsp65 IgG2a isotype production after WT or K(409)A injection, and LIII female groups showed no alterations.Conclusions: the results revealed that the WT Hsp65 interferes with survival of aged HIII female mice without involvement of a remarkable IgG1 and IgG2a anti-DNA and anti-Hsp65 antibodies production. the deleterious effects of Hsp65 on survival time in aged HIII female mice could be linked to a gender-effect and are in agreement with those previously reported in lupus-prone mice. en
dc.description.sponsorship National Institute of Science and Technology in Toxins (INCTTOX)
dc.description.sponsorship Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorship Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.format.extent 10
dc.language.iso eng
dc.publisher Biomed Central Ltd
dc.relation.ispartof Immunity & Ageing
dc.rights Acesso aberto
dc.subject Heat shock protein en
dc.subject Hsp65 en
dc.subject Aging en
dc.subject Immunosenescence en
dc.subject Antibody response en
dc.title Mycobacterium leprae Hsp65 administration reduces the lifespan of aged high antibody producer mice en
dc.type Artigo
dc.contributor.institution Inst Butantan
dc.contributor.institution Hosp Israelita Albert Einstein
dc.contributor.institution Universidade Federal de São Paulo (UNIFESP)
dc.description.affiliation Inst Butantan, Lab Imunoquim, BR-05530900 São Paulo, Brazil
dc.description.affiliation Hosp Israelita Albert Einstein, BR-05652000 São Paulo, Brazil
dc.description.affiliation Inst Butantan, Lab Imunogenet, BR-05530900 São Paulo, Brazil
dc.description.affiliation Universidade Federal de São Paulo, Dept Microbiol Immunol & Parasitol, BR-04023062 São Paulo, Brazil
dc.description.affiliationUnifesp Universidade Federal de São Paulo, Dept Microbiol Immunol & Parasitol, BR-04023062 São Paulo, Brazil
dc.description.sponsorshipID FAPESP: 2013/07467-1
dc.identifier.file WOS000335058900001.pdf
dc.identifier.doi 10.1186/1742-4933-11-6
dc.description.source Web of Science
dc.identifier.wos WOS:000335058900001



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