Human platelet aggregation is not altered by Shiga toxins 1 or 2.
The hemolytic uremic syndrome involves the presence of Shiga toxin producing strains of Escherichia coli and is associated with thrombocytopenia, platelet activation, and microthrombi formation. We have, therefore, investigated the ability of Shiga toxin isotypes 1 and 2 to cause or enhance platelet aggregation under resting or arterial-flow conditions using a sensitive quenched-flow system and single-particle counting. Incubation of platelets with Shiga toxins 1 or 2 at 10(-10) M or 10(-9) M for 0.5-2 hours failed to induce platelet aggregation under static or physiological flow conditions, either by themselves or in the presence of ADP or thrombin. Thus, these Shiga toxins do not appear to be able to influence platelet function directly, and their ability to cause platelet thrombi in vivo must result from indirect mechanisms.
Viisoreanu
D
D
Department of Biochemistry & Molecular Genetics, University of Virginia, School of Medicine, Charlottesville 22908, USA.
Polanowska-Grabowska
R
R
Suttitanamongkol
S
S
Obrig
T G
TG
Gear
A R
AR
D000244:Adenosine Diphosphate / Q000494:pharmacology; D001427:Bacterial Toxins / Q000494:pharmacology*; D002021:Buffers; D004305:Dose-Response Relationship, Drug; D006463:Hemolytic-Uremic Syndrome / Q000097:blood; D006801:Humans; D007700:Kinetics; D010974:Platelet Aggregation / Q000187:drug effects*; D022603:Shiga Toxins; D012965:Sodium Chloride / Q000494:pharmacology; D013917:Thrombin / Q000494:pharmacology; D013997:Time Factors
D001427:Bacterial Toxins; D002021:Buffers; D022603:Shiga Toxins; D012965:Sodium Chloride; D000244:Adenosine Diphosphate; D013917:Thrombin