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Related Experiment Videos

Lancefield group C Streptococcus milleri group strains aggregate human platelets

M D Willcox1, H J Oakey, D W Harty

  • 1Institute of Dental Research, United Dental Hospital of Sydney, NSW, Australia.

Microbial Pathogenesis
|June 1, 1994
PubMed
Summary

Certain Streptococcus milleri group (SMG) strains aggregate human platelets. This interaction involves a protein on the bacterial surface and is inhibited by substances affecting platelet function or bacterial aggregation.

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Area of Science:

  • Microbiology
  • Hematology
  • Bacterial Pathogenesis

Background:

  • Lancefield group C Streptococcus milleri group (SMG) strains are unique among SMG types for their ability to aggregate human platelets.
  • Platelet aggregation is a critical process in hemostasis and thrombosis, and bacterial interactions with platelets can influence disease pathogenesis.

Purpose of the Study:

  • To investigate the mechanism by which Lancefield group C SMG strains aggregate human platelets.
  • To identify the nature of the bacterial surface component responsible for platelet interaction.
  • To explore factors that inhibit this specific bacterial-induced platelet aggregation.

Main Methods:

  • Mixing bacterial cells and human platelets at an 8:1 ratio and observing aggregation over 10 minutes.
  • Testing the effect of various inhibitors, including cation chelators, cyclooxygenase pathway inhibitors, and ADP-depleting agents.

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  • Enzymatic and chemical treatments of bacterial cells, including protease, lipase, periodate, and antisera to Lancefield group C polysaccharide, to identify the interacting substance.

    • Main Results:

    • Complete platelet aggregation was observed within 10 minutes of mixing bacterial cells and platelets.
    • Substances that chelated cations, inhibited the cyclooxygenase pathway, reduced ADP availability, or disrupted platelet membrane stability inhibited bacterial aggregation of platelets.
    • Protease digestion of bacterial cells abolished aggregation, while lipase, periodate, or antisera treatments had no effect, indicating a proteinaceous nature of the interacting substance.

    Conclusions:

    • Lancefield group C SMG strains possess a proteinaceous surface component that mediates the aggregation of human platelets.
    • This interaction is sensitive to various factors affecting platelet activation and stability.
    • Understanding this mechanism may provide insights into bacterial pathogenesis and host-platelet interactions.