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Anthrax lethal and edema toxins fail to directly impair human platelet function.

Kassidy M Chauncey¹, Sarah E Szarowicz, Gurjit S Sidhu

¹Department of Medicine, University of Florida, Gainesville, FL 32610-0277, USA.

The Journal of Infectious Diseases

|December 14, 2011

Summary

Systemic anthrax-associated hemorrhage is not caused by anthrax toxins directly affecting human platelets. Toxin receptors on platelets are reduced, preventing toxin binding and entry.

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Area of Science:

Microbiology
Immunology
Toxicology

Background:

Systemic anthrax often presents with severe hemorrhage.
Anthrax toxins, specifically lethal toxin (LT) and edema toxin (ET), are key virulence factors.
The direct impact of these toxins on human platelets in the context of hemorrhage is not fully understood.

Purpose of the Study:

To investigate the effects of anthrax lethal toxin (LT) and edema toxin (ET) on human platelets.
To determine if LT and ET can bind to and enter human platelets.
To elucidate the role of platelet interactions with anthrax toxins in systemic anthrax-induced hemorrhage.

Main Methods:

Assessing the cleavage of mitogen-activated protein kinase 1 (MAPK1) by LT in human platelets.
Measuring intracellular cyclic adenosine monophosphate (cAMP) levels in human platelets treated with ET.
Quantifying the surface expression of toxin receptors (TEM8, CMG2) and coreceptor (LRP6) on human platelets.

Main Results:

LT did not cleave its target MAPK1 in human platelets.
ET failed to increase intracellular cAMP levels in human platelets.
Surface expression of TEM8, CMG2, and LRP6 was significantly reduced on human platelets, inhibiting toxin binding.

Conclusions:

Anthrax toxins do not directly cleave targets or alter signaling pathways within human platelets.
Reduced expression of key receptors and coreceptors prevents anthrax toxin binding to human platelets.
The direct action of anthrax toxins on human platelets is unlikely to be the cause of hemorrhage in systemic anthrax.