Related Experiment Video
Updated: Aug 13, 2026
A Simple Protocol for Platelet-mediated Clumping of Plasmodium falciparum-infected Erythrocytes in a Resource Poor Setting
Published on: May 16, 2013
Interaction of Histoplasma capsulatum with human platelets
Abstract:
Thrombocytopenia is a common accompaniment of disseminated histoplasmosis. The yeast form of Histoplasma capsulatum does not directly injure human platelets freed of plasma. Preincubation of H. capsulatum with plasma enabled it to induce prompt platelet aggregation and selective release of [3H]serotonin without release of lysosomal beta-glucuronidase and the cytoplasmic marker, lactate dehydrogenase. Platelet aggregation was mediated by adenosine diphosphate, as shown by the blocking of the reaction by apyrase. Indomethacin inhibited both aggregation and serotonin release, indicating their dependence on prostaglandin synthesis by platelets. Plasma IgG conferred [3H]serotonin-releasing activity after complexing with yeasts, and plasma fibrinogen was necessary for platelet aggregation; classical and alternative complement pathways were not involved. The interaction of H. capsulatum with human platelets, mediated by IgG and fibrinogen without complement, represents a new attribute of this fungal pathogen and may contribute to thrombocytopenia complicating disseminated histoplasmosis.
Insights
Disseminated histoplasmosis can cause low platelet counts. Histoplasma capsulatum yeasts interact with human platelets via plasma IgG and fibrinogen, leading to aggregation and serotonin release, contributing to thrombocytopenia.
Area of Science:
- Mycology
- Hematology
- Immunology
Background:
- Thrombocytopenia is frequently observed in disseminated histoplasmosis.
- The yeast form of Histoplasma capsulatum does not directly harm isolated human platelets.
Purpose of the Study:
- To investigate the mechanism by which Histoplasma capsulatum interacts with human platelets.
- To elucidate the role of plasma components and signaling pathways in H. capsulatum-induced platelet activation.
Main Methods:
- Platelet aggregation assays using H. capsulatum yeasts.
- Measurement of serotonin release and enzyme markers (beta-glucuronidase, lactate dehydrogenase).
- Inhibition studies using apyrase, indomethacin, and complement pathway modulators.
Main Results:
- Preincubation of H. capsulatum with plasma induced platelet aggregation and selective serotonin release.
- Platelet aggregation was mediated by adenosine diphosphate and required fibrinogen.
- Serotonin release depended on prostaglandin synthesis (inhibited by indomethacin) and was mediated by plasma IgG complexed with yeasts.
- Complement pathways were not involved.
Conclusions:
- Histoplasma capsulatum interacts with human platelets through a mechanism involving plasma IgG and fibrinogen, independent of complement.
- This interaction leads to platelet aggregation and serotonin release, potentially explaining the thrombocytopenia associated with disseminated histoplasmosis.
- This represents a novel pathogenic mechanism for H. capsulatum.
More Related Videos
05:49Procoagulant Platelet Characterization by Measuring Phosphatidylserine Exposure and Microvesicle Release from Human Purified Platelets
Published on: November 29, 2024
04:37Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation
Published on: May 23, 2025
Related Concept Videos
01:18Structure and Function of Platelets
Platelets are continually replenished, circulating in the bloodstream for 9-12 days before being removed by phagocytes, primarily in the spleen. A microliter of circulating blood contains between 150,000 and 450,000 platelets, with...
01:22Formation of the Platelet Plug
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...