Human Platelet Aggregation Is Not Altered by Shiga Toxins 1 or 2

• Published in: Thrombosis research Vol. 98; no. 5; pp. 403 - 410
• Main Authors: Viisoreanu, Delia, Polanowska-Grabowska, Renata, Suttitanamongkol, Sudawadee, Obrig, Tom G, Gear, Adrian R.L
• Format: Journal Article
• Language: English
• Published: New York, NY Elsevier Ltd 01.06.2000; Elsevier Science
• Subjects: Adenosine Diphosphate - pharmacology; Aggregation; Anemias. Hemoglobinopathies; Bacterial Toxins - pharmacology; Biological and medical sciences; Buffers; Diseases of red blood cells; Dose-Response Relationship, Drug; Hematologic and hematopoietic diseases; Hemolytic-Uremic Syndrome - blood; Humans; Kinetics; Medical sciences; Platelet Aggregation - drug effects; Platelets; Shiga Toxins; Sodium Chloride - pharmacology; Thrombin - pharmacology; Time Factors; Aggregation; BSA, bovine serum albumin; PBS, phosphate-buffered saline; PRP, platelet-rich plasma; FITC, fluorescein isothiocyanate; Stx, Shiga toxin; Shiga toxins; HUS, hemolytic uremic syndrome; Platelets; ACD, acid-citrate-dextrose; SFLLR, thrombin-receptor activating peptide; PPP, platelet-poor plasma; Kidney disease; Human; Urinary system disease; Hemolytic uremic syndrome; Pathogenesis; Escherichia coli; Shigella dysenteriae; Hemopathy; Shiga-like toxin; Blood cell; Platelet; Hemolytic anemia; Renal failure; Bacteria; Enterobacteriaceae
• ISSN: 0049-3848; 1879-2472
• DOI: 10.1016/S0049-3848(00)00191-2

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.