Modulation of angiogenic factor VEGF by DNA-hsp65 vaccination in a murine CNS tuberculosis model
Autor: | Osvaldo Massaiti Takayanagui, Adriana Pelegrini-da-Silva, Fabiola C. R. Zucchi, Célio Lopes Silva, Ana Maria C. Tsanaclis, Quintino Moura-Dias, Luciano Neder |
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Rok vydání: | 2013 |
Předmět: |
Male
Vascular Endothelial Growth Factor A Microbiology (medical) Tuberculosis Angiogenesis Immunology Vascular permeability Microbiology Tuberculous meningitis Mice chemistry.chemical_compound Bacterial Proteins Antigen Cerebellar Diseases Cerebellum MODELOS ANIMAIS DE DOENÇAS Vaccines DNA Animals Medicine Tuberculosis Vaccines Immunization Schedule Mycobacterium bovis biology business.industry Chaperonin 60 Tuberculosis Central Nervous System biology.organism_classification medicine.disease Vaccination Vascular endothelial growth factor Disease Models Animal Infectious Diseases Tuberculoma Intracranial chemistry Tuberculosis Meningeal business |
Zdroj: | Repositório Institucional da USP (Biblioteca Digital da Produção Intelectual) Universidade de São Paulo (USP) instacron:USP |
ISSN: | 1472-9792 |
DOI: | 10.1016/j.tube.2013.02.002 |
Popis: | summary Tuberculosis (TB) is a serious public health problem. Development of experimental models and vaccines are essential to elucidate physiopathological mechanisms and to control the disease. Vascular endothelial growth factor (VEGF) is a potent activator of vascular permeability and angiogenesis. VEGF seems to participate in breakdown of the blood brain-barrier (BBB) in tuberculous meningitis (TBM), contributing to worsening of disease. Therefore, the objective here was to extent the characterization of our previously described murine model of central nervous system TB (CNS-TB) by describing the VEGF participation in the CNS disease, and suggesting a vaccination plan in mice. Plasmid encoding DNA protein antigen DNAhsp65 has been described as a protector against TB infection and was used here to test its effectiveness in the prevention of VEGF production and TB disease. Vaccinated mice and its controls were injected with Mycobacterium bovis bacillus Calmette-Guerin (BCG) in cerebellum. Four weeks after BCG injection, mice were perfused and brains were paraffin-embedded for VEGF expression analysis. We observed VEGF immunohistochemical expression in TBM and granulomas in non-vaccinated mice. The DNA-hsp65 treatment blocked the expression of VEGF in mice TBM. Therefore, our murine model indicated the VEGF participation in the physiopathology of CNS-TB and the potential prevention of the DNA-hsp65 in the disease progression. |
Databáze: | OpenAIRE |
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