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Effect of pathogenic yeasts on human platelet aggregation

Teresinha de Jesus Carvalho Neiva1, Jairo Ivo dos Santos

  • 1Federal University of Santa Catarina, Centre of Health Science, Florianópolis, SC, Brazil. neiva@ccs.ufsc.br

The Brazilian Journal of Infectious Diseases : an Official Publication of the Brazilian Society of Infectious Diseases
|November 26, 2003
PubMed

Insights

Fungal cells from Candida albicans and Cryptococcus neoformans inhibit human platelet aggregation (PA). This effect stems from yeast components, not secreted products, potentially aiding fungal evasion of immune defenses.

Area of Science:

  • Mycology
  • Immunology
  • Hematology

Background:

  • Candida albicans and Cryptococcus neoformans are opportunistic fungal pathogens.
  • Fungal dissemination often involves interactions with the host's circulatory system.
  • Platelet aggregation (PA) plays a role in hemostasis and immune responses.

Purpose of the Study:

  • To investigate the impact of C. albicans and C. neoformans on human platelet aggregation (PA).
  • To determine if direct yeast-cell contact or secreted factors are responsible for any observed effects on PA.

Main Methods:

  • Human platelets were subjected to aggregation assays.
  • Platelet aggregation was measured in the presence of varying concentrations of C. albicans and C. neoformans cells.
  • Platelet aggregation was also assessed with the addition of yeast culture supernatants.

Main Results:

  • Neither C. albicans nor C. neoformans directly induced platelet aggregation.
  • Yeast cells significantly inhibited PA at concentrations of 1 x 10^6 cells/mL (C. albicans) and 1 x 10^5 cells/mL (C. neoformans).
  • Culture supernatants from both yeasts did not inhibit platelet aggregation.

Conclusions:

  • Somatic components of C. albicans and C. neoformans, not their metabolic products, antagonize human platelet aggregation.
  • This interaction may represent a mechanism for fungal immune evasion during vascular dissemination.

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