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Induction of procoagulant activity on human endothelial cells by Streptococcus pneumoniae

S Geelen1, C Bhattacharyya, E Tuomanen

  • 1Laboratory of Molecular Infectious Diseases, Rockefeller University, New York, New York 10021.

Infection and Immunity
|October 1, 1992
PubMed

Insights

Gram-positive bacteria, specifically pneumococci, trigger procoagulant activity (PCA) in human endothelial cells. This finding reveals a new role for bacterial cell walls in the inflammatory response and thrombosis.

Area of Science:

  • Microbiology
  • Immunology
  • Hematology

Background:

  • Gram-negative infections induce procoagulant activity (PCA) in endothelial cells, contributing to inflammation and thrombosis.
  • While Gram-positive infections also involve fibrin formation, the specific bacterial factors responsible for inducing PCA remain unidentified.

Purpose of the Study:

  • To investigate whether Gram-positive organisms, specifically *Streptococcus pneumoniae* (pneumococci), can induce PCA on human endothelial cells.
  • To identify the bacterial components of pneumococci responsible for inducing PCA.

Main Methods:

  • Human endothelial cells were exposed to intact pneumococci (encapsulated and unencapsulated strains) and purified pneumococcal cell walls.
  • Procoagulant activity (PCA) was measured over time (30 min to 6 h) following exposure.
  • The potency of pneumococcal cell walls in inducing PCA was compared to endotoxin.

Main Results:

  • Intact pneumococci and purified pneumococcal cell walls efficiently induced PCA on human endothelial cells.
  • PCA was detectable within 30 minutes, peaked at 2 hours, and diminished by 6 hours.
  • Encapsulated and unencapsulated pneumococcal strains showed equivalent PCA induction. Purified pneumococcal cell walls were as potent as endotoxin in inducing PCA.

Conclusions:

  • Gram-positive bacterial cell walls, exemplified by pneumococcal cell walls, possess the novel ability to induce PCA on endothelial cells.
  • This procoagulant effect of Gram-positive cell walls contributes to the coagulation cascade's involvement in the inflammatory response to Gram-positive infections.
  • The findings identify a new mechanism linking Gram-positive bacterial infections to thrombotic complications.

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