The aggregation of human platelets by Lactobacillus species.
The ability to aggregate human platelets was examined for five Lactobacillus rhamnosus strains and five Lactobacillus paracasei subsp. paracasei 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 Lactobacillus acidophilus, Lactobacillus fermentum, Lactobacillus oris, Lactobacillus plantarum and Lactobacillus salivarius. Amongst the L. rhamnosus strains, platelets were aggregated by all five IE strains and 8/16 laboratory strains. For the L. paracasei subsp. paracasei 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 +/- 0.1 and 20.4 +/- 3.2 min and the percentage aggregation ranged between 70 +/- 2.6 and 104 +/- 13.5%. 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 L. rhamnosus 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 degrees C for 1 h stopped aggregation in 8/9 IE strains. Extracted surface proteins (200 micrograms) completely inhibited platelet aggregation by 8/9 of the homologous strains.(ABSTRACT TRUNCATED AT 250 WORDS)
Harty
D W
DW
Institute of Dental Research, Surry Hills, NSW, Australia.
Patrikakis
M
M
Hume
E B
EB
Oakey
H J
HJ
Knox
K W
KW
D016470:Bacteremia / Q000209:etiology / Q000382:microbiology; D002462:Cell Membrane / Q000502:physiology; D004697:Endocarditis, Bacterial / Q000209:etiology / Q000382:microbiology; D006801:Humans; D066298:In Vitro Techniques; D007778:Lactobacillus / Q000187:drug effects / Q000302:isolation & purification / Q000472:pathogenicity*; D009055:Mouth / Q000382:microbiology; D010974:Platelet Aggregation / Q000187:drug effects / Q000502:physiology*; D010975:Platelet Aggregation Inhibitors / Q000494:pharmacology; D013045:Species Specificity
D010975:Platelet Aggregation Inhibitors