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Related Experiment Video

Updated: Jun 30, 2025

A Murine Model of Group B Streptococcus Vaginal Colonization
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Specific interaction between Group B Streptococcus CC17 hypervirulent clone and phagocytes.

Anne-Sophie Bourrel1,2, Amandine Picart1, Jose-Carlos Fernandez1

  • 1Université Paris Cité, Institut Cochin, INSERM, U1016, CNRS, UMR8104, Paris, France.

Infection and Immunity
|March 22, 2024
PubMed
Summary
This summary is machine-generated.

Hypervirulent Group B Streptococcus (GBS) CC17 strains attach to and are phagocytosed by macrophages more readily than other GBS strains, mediated by specific surface proteins. This enhanced interaction may aid GBS CC17 persistence and dissemination.

Keywords:
CC17Group BStreptococcusStreptococcus agalactiaeTHP-1adhesionphagocytosis

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Area of Science:

  • Immunology
  • Microbiology
  • Infectious Diseases

Background:

  • Group B Streptococcus (GBS) is a major cause of neonatal invasive infections.
  • The capsular serotype III clonal complex 17 (CC17) of GBS is a hypervirulent clone strongly associated with neonatal meningitis.
  • Macrophages serve as a permissive intracellular niche for GBS survival.

Purpose of the Study:

  • To investigate the specific interactions between hypervirulent GBS CC17 strains and macrophages.
  • To elucidate the mechanisms underlying the enhanced interaction of GBS CC17 with host immune cells.

Main Methods:

  • Comparative analysis of GBS CC17 and non-CC17 strain phagocytosis by human monocytes and macrophages.
  • Investigation of the role of the HvgA protein and PI-2b pilus (Spb1) in GBS CC17 adhesion.
  • Assessment of scavenger receptor involvement using inhibitors (fucoidan, poly(I)).
  • Analysis of intracellular bacterial survival and egress mechanisms.

Main Results:

  • GBS CC17 strains exhibit significantly higher adhesion and phagocytosis rates by macrophages compared to non-CC17 strains.
  • Enhanced CC17 phagocytosis is mediated by the surface protein HvgA and the PI-2b pilus (Spb1), interacting with scavenger receptors.
  • Intracellular survival and egress mechanisms were similar for both CC17 and non-CC17 strains within macrophages.

Conclusions:

  • The hypervirulent GBS CC17 clone possesses a unique capacity for enhanced adhesion and phagocytosis by macrophages.
  • This enhanced interaction, driven by specific surface factors, may contribute to the persistence and dissemination of GBS CC17 within the host.
  • Understanding these interactions provides insights into host immune subversion by pathogenic bacteria.