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Binding of resting platelets to Candida albicans germ tubes
R Robert1, C Mahaza, M Miegeville
1Laboratoire d'Immunologie-Mycologie-Bactériologie, UFR des Sciences Médicales et Pharmaceutiques, Angers, France.
Infection and Immunity
|September 1, 1996
Summary
Resting platelets specifically bind to Candida albicans germ tubes via a fungal protein receptor. This interaction causes significant platelet shape changes, indicating a direct adhesion mechanism.
Area of Science:
- Mycology
- Hematology
- Immunology
Background:
- Candida albicans is an opportunistic fungal pathogen that can cause systemic infections.
- Platelets play a role in host defense and inflammation beyond hemostasis.
- The interaction between platelets and C. albicans is not fully understood.
Purpose of the Study:
- To investigate the specific binding mechanism between resting human platelets and Candida albicans germ tubes.
- To identify the nature of the interaction and any associated cellular changes.
Main Methods:
- Utilized an affinity column with immobilized Candida albicans germ tubes to study platelet adhesion.
- Quantified platelet binding based on germ tube and platelet concentrations.
- Employed scanning electron microscopy (SEM) to visualize platelet-fungus interactions and morphological changes.
Main Results:
- Platelet adhesion to germ tubes was concentration-dependent, suggesting a specific interaction.
- Evidence points to a fungal protein receptor mediating the specific binding of platelets to C. albicans germ tubes.
- SEM confirmed direct platelet attachment and revealed significant morphological alterations in platelets, including shape change, pseudopod formation, and flattening.
Conclusions:
- Resting platelets exhibit specific adhesion to Candida albicans germ tubes.
- The interaction is mediated by a fungal protein receptor on the germ tube.
- Platelet activation and morphological changes occur upon binding to C. albicans.