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Invasion of Human Cells by a Bacterial Pathogen
07:15

Invasion of Human Cells by a Bacterial Pathogen

Published on: March 21, 2011

A STUDY ON THE MECHANISM OF INVASIVENESS OF STREPTOCOCCI

E W Dennis1, D Berberian

  • 1Department of Bacteriology, School of Medicine, American University of Beirut, Beirut, Lebanon.

The Journal of Experimental Medicine
|October 30, 2009
PubMed

Insights

Streptococcus haemolyticus produces fibrinolytic and antifibrinogenic substances that prevent clot formation, aiding bacterial spread. These factors are thermostable, antigenic, and correlate with streptococcal invasiveness.

Area of Science:

  • Microbiology
  • Immunology
  • Pathology

Background:

  • Inflammatory fixation is crucial for limiting pathogen spread.
  • Streptococcus haemolyticus infections can overcome this defense mechanism.

Purpose of the Study:

  • To confirm Menkin's findings on the failure of inflammatory fixation in Streptococcus haemolyticus infections.
  • To investigate the mechanisms by which streptococci evade inflammatory responses.

Main Methods:

  • Confirmation of previous observations regarding inflammatory fixation.
  • Analysis of bacterial products responsible for interfering with fibrin barrier formation.
  • Assessment of the thermostability and antigenicity of these substances.
  • Correlation studies between substance production and bacterial invasiveness.

Main Results:

  • The failure of inflammatory fixation is confirmed in acute Streptococcus haemolyticus infections.
  • Streptococci produce fibrinolytic and antifibrinogenic substances that prevent fibrin barrier formation.
  • These substances maintain lymphatic and capillary patency, facilitating bacterial dissemination.
  • The production of these substances correlates with the invasiveness of Streptococcus strains.
  • Both substances are relatively thermostable and appear to be antigenic with type specificity.

Conclusions:

  • Fibrinolytic and antifibrinogenic substances produced by Streptococcus haemolyticus are key factors in its invasiveness.
  • These bacterial products disrupt the host's inflammatory response by preventing fibrin clot formation.
  • Understanding these mechanisms can inform strategies to combat streptococcal infections.

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