Use este identificador para citar ou linkar para este item: https://locus.ufv.br//handle/123456789/18386
Tipo: Artigo
Título: Differential cellular immune response of Galleria mellonella to Actinobacillus pleuropneumoniae
Autor(es): Blanco, Luis Andrés Arteaga
Crispim, Josicelli Souza
Fernandes, Kenner Morais
Oliveira, Leandro Licursi de
Pereira, Monalessa Fábia
Bazzolli, Denise Mara Soares
Martins, Gustavo Ferreira
Abstract: In the present work, we have investigate the cellular immune response of Galleria mellonella larvae against three strains of the gram-negative bacterium Actinobacillus pleuropneumoniae: low-virulence (780), high-virulence (1022) and the serotype 8 reference strain (R8). Prohemocytes, plasmatocytes, granulocytes, oenocytoids and spherulocytes were distinguished according to their size and morphology, their molecular markers and dye-staining properties and their role in the immune response. Total hemocyte count, differential hemocyte count, lysosome activity, autophagic response, cell viability and caspase-3 activation were determined in circulating hemocytes of naive and infected larvae. The presence of the autophagosome protein LC3 A/B within the circulating hemocytes of G. mellonella was dependent on and related to the infecting A. pleuropneumoniae strain and duration of infection. Hemocytes treated with the high-virulence strain expressed higher levels of LC3 A/B, whereas treatment with the low-virulence strain induced lower expression levels of this protein in the cells. Moreover, our results showed that apoptosis in circulating hemocytes of G. mellonella larvae after exposure to virulent bacterial strains occurred simultaneously with excessive cell death response induced by stress and subsequent caspase-3 activation.
Palavras-chave: Apoptosis
Autophagy
Immune response
Actinobacillus pleuropneumoniae
Galleria mellonella
Editor: Cell and Tissue Research
Tipo de Acesso: Springer Berlin Heidelberg
URI: https://doi.org/10.1007/s00441-017-2653-5
http://www.locus.ufv.br/handle/123456789/18386
Data do documento: 8-Jul-2017
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