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Related Experiment Videos

Group B streptococci persist inside macrophages

P Cornacchione1, L Scaringi, K Fettucciari

  • 1Department of Clinical Medicine, Pathology and Pharmacology, University of Perugia, Italy.

Immunology
|April 16, 1998
PubMed
Summary
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Group B streptococci (GBS) survive inside macrophages, evading immune responses. This study shows GBS impairs protein kinase C (PKC) signaling, aiding their intracellular persistence and contributing to GBS infections.

Area of Science:

  • Immunology
  • Microbiology
  • Cell Biology

Background:

  • Group B streptococci (GBS) are a significant cause of neonatal infections like sepsis, pneumonia, and meningitis.
  • Macrophages and polymorphonuclear cells (PMN) are crucial in the initial immune response to GBS.
  • Understanding GBS-macrophage interactions is key to developing therapeutic strategies, especially in the absence of antibodies.

Purpose of the Study:

  • To investigate GBS survival within macrophages in vitro, without type-specific antibodies.
  • To determine the impact of GBS on the protein kinase C (PKC)-dependent signaling pathway in macrophages.
  • To elucidate the role of PKC in intracellular GBS survival and macrophage antimicrobial function.

Main Methods:

  • In vitro phagocytosis of GBS strains (type Ia and type III) by murine peritoneal macrophages.

Related Experiment Videos

  • Assessment of GBS intracellular survival over time (24-48 hours).
  • Macrophage activation using interferon-gamma (IFN-gamma) and lipopolysaccharide (LPS).
  • Modulation of PKC activity using phorbol 12-myristate 13-acetate (PMA) and Calphostin C.
  • Evaluation of macrophage antimicrobial activity and c-fos gene expression post-stimulation.

    • Main Results:

    • GBS strains Ia and III survived intracellularly in macrophages for extended periods (24-48 hours).
    • Macrophage activation with IFN-gamma and LPS reduced GBS intracellular persistence.
    • PKC depletion or inhibition increased macrophage permissiveness to GBS survival.
    • GBS-infected macrophages showed impaired antimicrobial responses to PMA and LPS.
    • GBS infection led to reduced c-fos gene expression, indicating impaired PKC signaling.

    Conclusions:

    • GBS can survive and persist within macrophages, contributing to infection pathogenesis.
    • Impairment of the PKC signal transduction pathway by GBS is a mechanism for their intracellular survival.
    • Targeting PKC signaling could be a potential strategy to enhance macrophage defense against GBS.