SUMMARY: The ability to aggregate human platelets was examined for five strains and five subsp. strains isolated from patients with infective endocarditis (IE), 25 laboratory isolates from the same two species, and 14 strains from five other oral species, namely and Amongst the strains, platelets were aggregated by all five IE strains and 8/16 laboratory strains. For the subsp. strains, the respective numbers were 2/5 and 2/9. Aggregation also occurred with 11/14 strains of the other five species; each species was represented. The optimal ratio of bacteria to platelets for aggregation was approximately 1:1, and there was considerable variation in the lag phase that preceded aggregation, depending on the source of the platelets. Overall, the lag phase varied between 0.25±pL0.1 and 20.4±pL3.2 min and the percentage aggregation ranged between 70±pL2.6 and 104±pL13.5%. Confirmation that aggregation was being observed came from studies with five strains on the inhibitory effects of EDTA, dipyridamole, apyrase, imipramine, acetylsalicylic acid and quinacrine. Inhibition of aggregation by strains by the peptide arginine-glycine-aspartic acid-serine (RGDS) further indicated a role for fibronectin and/or fibrinogen. Pronase treatment of cells for 1 h and extraction of bacterial surface components with 0.1 M-Tris/HCl (pH 8.5) at 37 °dGC for 1 h stopped aggregation in 8/9 IE strains. Extracted surface proteins (200 μg) completely inhibited platelet aggregation by 8/9 of the homologous strains. A comparison of the platelets from four donors showed that an increase in the lag phase by 50% required 11.5, 14.8, 33.3 or 115 μg of extract, indicating a variability in donor response to aggregation by lactobacilli. The data indicate that platelet aggregation by lactobacilli may be an important contributory factor in IE. The potential to cause IE is present in the general population of oral lactobacilli and due regard should be taken when strain selection is made for probiotic purposes.


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