BCG and BCG/DNAhsp65 Vaccinations Promote Protective Effects without Deleterious Consequences for Experimental Autoimmune Encephalomyelitis


Autoria(s): Goncalves Zorzella-Pezavento, Sofia Fernanda; Fujiara Guerino, Clara Pires; Chiuso-Minicucci, Fernanda; Donega Franca, Thais Graziela; Watanabe Ishikawa, Larissa Lumi; Masson, Ana Paula; Silva, Celio Lopes; Sartori, Alexandrina
Contribuinte(s)

Universidade Estadual Paulista (UNESP)

Data(s)

03/12/2014

03/12/2014

01/01/2013

Resumo

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Processo FAPESP: 07/05353-8

A prime-boost strategy conserving BCG is considered the most promising vaccine to control tuberculosis. A boost with a DNA vaccine containing the mycobacterial gene of a heat shock protein (pVAXhsp65) after BCG priming protected mice against experimental tuberculosis. However, anti-hsp65 immunity could worsen an autoimmune disease due to molecular mimicry. In this investigation, we evaluated the effect of a previous BCG or BCG/pVAXhsp65 immunization on experimental autoimmune encephalomyelitis (EAE) development. Female Lewis rats were immunized with BCG or BCG followed by pVAXhsp65 boosters. The animals underwent EAE induction and were daily evaluated for weight loss and clinical score. They were euthanized during recovery phase to assess immune response and inflammatory infiltration at the central nervous system. Previous immunization did not aggravate or accelerate clinical score or weight loss. In addition, this procedure clearly decreased inflammation in the brain. BCG immunization modulated the host immune response by triggering a significant reduction in IL-10 and IFN-gamma levels induced by myelin basic protein. These data indicated that vaccination protocols with BCG or BCG followed by boosters with pVAXhsp65 did not trigger a deleterious effect on EAE evolution.

Formato

9

Identificador

http://dx.doi.org/10.1155/2013/721383

Clinical & Developmental Immunology. New York: Hindawi Publishing Corporation, 9 p., 2013.

1740-2522

http://hdl.handle.net/11449/112632

10.1155/2013/721383

WOS:000326839000001

WOS000326839000001.pdf

Idioma(s)

eng

Publicador

Hindawi Publishing Corporation

Relação

Clinical & Developmental Immunology

Direitos

openAccess

Tipo

info:eu-repo/semantics/article