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Stepping Up to the Plate(let) against Candida albicans
Christina M Schultz1, Arukshita Goel1, Allison Dunn1
1Department of Medical Microbiology and Immunology, University of Toledo College of Medicine and Life Sciences, Toledo, Ohio, USA.
Abstract:
Candida albicans is a pervasive commensal fungus that is the most common pathogen responsible for invasive fungal infection (IFI). With incidence of IFI on the rise due to increasing susceptible populations, it is imperative that we investigate how Candida albicans interacts with blood components. When stimulating either human or mouse whole blood with thrombin, we saw a significant decrease in C. albicans survival. We then repeated Candida killing assays with thrombin-stimulated or unstimulated washed platelets and saw a similar decrease in CFU. To investigate whether killing was mediated through surface components or releasable products, platelets were pretreated with an inhibitor of actin polymerization (cytochalasin D [CytoD]). CytoD was able to abrogate C. albicans killing. Moreover, dilution of releasates from thrombin-stimulated platelets showed that the toxicity of the releasates on C. albicans is concentration dependent. We then investigated C. albicans actions on platelet activation, granule release, and aggregation. While C. albicans does not appear to affect alpha or dense granule release, C. albicans exerts a significant attenuation of platelet aggregation to multiple agonists. These results illustrate for the first time that platelets can directly kill C. albicans through release of their granular contents. Additionally, C. albicans can also exert inhibitory effects on platelet aggregation.
Insights
Platelets kill Candida albicans by releasing granular contents, a process dependent on actin polymerization. Candida albicans also inhibits platelet aggregation, revealing a complex interaction between these two key components.
Area of Science:
- Hematology
- Mycology
- Immunology
Background:
- Candida albicans is a common fungal pathogen causing invasive fungal infections (IFIs).
- Increasing numbers of susceptible individuals necessitate understanding Candida albicans interactions with blood components.
- Platelets are key immune cells involved in hemostasis and immunity.
Purpose of the Study:
- To investigate the interaction between Candida albicans and human/mouse blood components, particularly platelets.
- To determine if platelets can kill Candida albicans and elucidate the mechanisms involved.
- To assess the impact of Candida albicans on platelet function, including aggregation and granule release.
Main Methods:
- Candida albicans survival assays were performed using thrombin-stimulated whole blood and washed platelets.
- Platelets were pretreated with cytochalasin D (CytoD), an inhibitor of actin polymerization, to assess killing mechanisms.
- Releasates from stimulated platelets were tested for toxicity against Candida albicans in a concentration-dependent manner.
- Candida albicans effects on platelet activation, alpha/dense granule release, and aggregation were evaluated.
Main Results:
- Thrombin stimulation of whole blood and platelets significantly decreased Candida albicans survival.
- Platelet-mediated killing of Candida albicans was abrogated by cytochalasin D, indicating dependence on actin polymerization.
- Toxicity of platelet releasates on Candida albicans was concentration-dependent.
- Candida albicans significantly attenuated platelet aggregation induced by various agonists but did not affect alpha or dense granule release.
Conclusions:
- Platelets possess the capacity to directly kill Candida albicans through the release of granular contents.
- This platelet-mediated killing mechanism is dependent on actin polymerization.
- Candida albicans can modulate platelet function by inhibiting platelet aggregation.
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