Inhibitory effects of lipoteichoic acid from Staphylococcus aureus on platelet function and platelet–monocyte aggregation

Abstract

Lipoteichoic acid (LTA) from Staphylococcus aureus has been demonstrated to inhibit agonist-stimulated platelet aggregation. However, its effects on platelet inflammatory mediator release and platelet-monocyte aggregation are still unclear. In the present study, LTA is examined for its anti-inflammatory properties and effects on platelet-monocyte aggregation. Blood samples were obtained from 5 healthy volunteers who had taken no medicine in the previous 2weeks. Washed platelets were prepared and incubated with LTA (0.5-2.0μg/mL), then platelet aggregation, P-selectin expression, and soluble CD40L (sCD40L) release were measured by light transmission aggregometry, flow cytometry and enzyme-linked immunoassays, respectively. Platelet-monocyte aggregate formation in whole blood was measured by flow cytometry. Thrombin was used as a stimulant. LTA dose-dependently decreased platelet aggregation from 89.32±10.24% to 36.28±9.01% (P<0.05), sCD40L release from 3.28±0.76 to 1.13±0.45ng/mL (P<0.05) and surface P-selectin expression from 82.01±11.20 to 22.78±6.42% (P<0.05). In human whole blood, 1.0μg/mL LTA inhibited platelet-monocyte aggregation from 78.19±10.94 to 38.24+8.74% (P<0.05). These results indicate that LTA from S. aureus can inhibit platelet-dependent inflammatory mediator release and platelet-monocyte aggregation. These findings suggest that LTA-mediated functional alteration of platelets may contribute to immune evasion of S. aureus.