PubMed HealthSearch

PubMed · 6403459

Platelet aggregation by Streptococcus pyogenes.

Abstract

Heat-killed group A Streptococcus pyogenes induced platelet aggregation in platelet-rich plasma. Aggregation was dependent upon the ratio of platelets to bacteria, with maximal aggregation occurring at 0.8 platelets per bacterium (final concentration, 300,000 per microliter). Inhibition of the reaction by 3 mM EDTA indicated it was a true aggregation and not merely adhesion and agglutination. Lactic acid dehydrogenase assays indicated lysis of platelets did not occur during a 6-min incubation period. Aggregation was inhibited in a dose-dependent manner by acetylsalicylic acid (100 microM to 10 mM) and quinacrine (15.6 to 250 microM), with no decrease in aggregation at the lowest concentration of inhibitor tested. S. pyogenes induced the release of [14C]serotonin, which was maximal (50%) at 2.4 min, when aggregation was nearly complete. Gel-filtered platelets were not aggregated unless fibrinogen (final concentration, 1.8 mg/ml) was included in the reaction mixture. Staphylococcus aureus, a group B streptococcus, and Escherichia coli were unable to induce aggregation in platelet-rich plasma under the conditions used for S. pyogenes.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

G E Kurpiewski, L J Forrester, B J Campbell, J T Barrett. 1983. Platelet aggregation by Streptococcus pyogenes.. https://doi.org/10.1128/iai.39.2.704-708.1983

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Medical compared with surgical treatment of asymptomatic carotid artery stenosis.

The Asymptomatic Carotid Atherosclerosis Study (ACAS) results suggest that carotid endarterectomy combined with aspirin and risk factor reduction is superior to aspirin and risk factor reduction is superior to aspirin and risk factor reduction alone in preventing ipsilateral stroke in asymptomatic patients with diameter stenosis of the carotid artery of 60% or more. The absolute risk reduction over 5 years conferred by surgical therapy is modest (5.9%) compared with the risk reduction conferred by surgical therapy for symptomatic carotid disease but compares favorably with the degree of stroke prevention shown for antihypertensive therapy in the elderly. For prevention of stroke in women and for prevention of major stroke, the ACAS results favoring surgery did not reach statistical significance. The combined arteriographic and perioperative surgery-related mortality and stroke rates achieved by the carefully selected surgical teams was low (2.3%). Accordingly, carotid endarterectomy can be recommended for preventing stroke in the setting of hemodynamically significant stenosis when the arteriographic and surgical complication rates can be kept low.

Aspirin

Thrombopoietin, c-Mpl ligand, induces tyrosine phosphorylation of Tyk2, JAK2, and STAT3, and enhances agonists-induced aggregation in platelets in vitro.

We investigated in vitro effects of recombinant human thrombopoietin (TPO), or c-Mpl ligand, on human platelets. TPO induced rapid dose-dependent tyrosine phosphorylation of several proteins. We identified Janus tyrosine kinases, Tyk2 and JAK2, and a member of STAT (signal transducers and activators of transcription) family, STAT3, as the tyrosine-phosphorylated proteins in response to TPO. TPO by itself did not cause platelet aggregation and shape change, but augmented ADP-induced aggregation in a dose-dependent manner. Acetylsalicylic acid inhibited the secondary aggregation enhanced by TPO, but not the TPO-induced potentiation of the primary aggregation. TPO modulates platelet activation possibly through protein-tyrosine phosphorylation.

Aspirin