Figure 4.
Figure 4. Mechanism of S agalactiae–induced platelet activation/aggregation. (A) Effect of inhibitors on S agalactiae 6313-induced platelet aggregation. PRP (0.4 mL) was pretreated with 1 mM RGDS, abciximab (10 μg/mL), 1 μM PGE1, or apyrase (10 U/mL) for 5 minutes or with 1 μM ASA for 20 minutes prior to the induction of platelet aggregation by 10 μM ADP (▪) or S agalactiae 6313 cells (5 × 107; □). Results are expressed as percentage of aggregation performed in the absence of antagonists. Each data point is the mean ± SD of 4 experiments. (B) S agalactiae cells induce cytosolic Ca2+ increase in platelets. Fura-2/am-loaded platelets (8 × 107 in 0.4 mL) were stimulated with 2.5 × 105 or 2.5 × 106 cells of S agalactiae 6313 in the presence of Fbg (3 mg/mL). Trace of Ca2+ increase by thrombin (1 U/mL) is shown as control. The effect of either bacteria or Fbg on Ca2+ increase in platelets is also reported. The arrows indicate the addition of agonist to platelets. Results are representative of 3 experiments.

Mechanism ofS agalactiae–induced platelet activation/aggregation. (A) Effect of inhibitors on S agalactiae 6313-induced platelet aggregation. PRP (0.4 mL) was pretreated with 1 mM RGDS, abciximab (10 μg/mL), 1 μM PGE1, or apyrase (10 U/mL) for 5 minutes or with 1 μM ASA for 20 minutes prior to the induction of platelet aggregation by 10 μM ADP (▪) or S agalactiae 6313 cells (5 × 107; □). Results are expressed as percentage of aggregation performed in the absence of antagonists. Each data point is the mean ± SD of 4 experiments. (B) S agalactiae cells induce cytosolic Ca2+ increase in platelets. Fura-2/am-loaded platelets (8 × 107 in 0.4 mL) were stimulated with 2.5 × 105 or 2.5 × 106 cells of S agalactiae 6313 in the presence of Fbg (3 mg/mL). Trace of Ca2+ increase by thrombin (1 U/mL) is shown as control. The effect of either bacteria or Fbg on Ca2+ increase in platelets is also reported. The arrows indicate the addition of agonist to platelets. Results are representative of 3 experiments.

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