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Mechanisms of group b streptococcal-induced apoptosis of murine macrophages

Academic Article
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Overview

authors

  • Ulett, G. C.
  • Maclean, K. H.
  • Nekkalapu, S.
  • Cleveland, John
  • Adderson, E. E.

publication date

  • August 2005

journal

  • Journal of Immunology  Journal

abstract

  • Apoptosis of murine and human macrophages induced by group B Streptococcus agalactiae (GBS) is likely an important virulence mechanism that is used by the bacteria to suppress the host immune response and to persist at sites of infection. The mechanisms by which GBS induces apoptosis are, however, largely unknown. In this study, we report that in murine macrophages GBS induces unique changes in the regulation and localization of the apoptotic regulators Bad, 14-3-3, and Omi/high-temperature requirement A2 and leads to the release of cytochrome c and the activation of caspase-9 and caspase-3. Furthermore, inhibition of caspase-3 impaired GBS-induced apoptosis of macrophages. The ability to modulate the activity of effector caspases may therefore represent an unexploited avenue for therapeutic intervention in GBS infections.

subject areas

  • 14-3-3 Proteins
  • Animals
  • Apoptosis
  • Caspase 3
  • Caspase 9
  • Caspase Inhibitors
  • Caspases
  • Cell Line
  • Cytochromes c
  • Enzyme Activation
  • Macrophages
  • Macrophages, Peritoneal
  • Mice
  • Mice, Inbred C57BL
  • Mitochondria
  • Mitochondrial Proteins
  • Serine Endopeptidases
  • Streptococcus agalactiae
  • bcl-Associated Death Protein
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Identity

International Standard Serial Number (ISSN)

  • 0022-1767

PubMed ID

  • 16081829
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Additional Document Info

start page

  • 2555

end page

  • 2562

volume

  • 175

issue

  • 4

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