Figure 4
Figure 4. Anti–P-selectin antibodies completely inhibit H pylori–induced platelet aggregation. Before the addition of H pylori (platelet/bacteria ratio = 25:1) and aggregation activators, anti-CD62P antibodies were incubated with PRP for 1 minute. (A) Addition of anti-CD62P antibodies was found to inhibit aggregations induced by pro-aggregatory Hp 49503, AA, and epinephrine. PRP, washed platelets, and pooled Igs were obtained from the anti-Hp antibody-positive samples. Washed platelets were prepared by resuspending the pellets of PRP mixture in N-2-hydroxyethylpiperazine-N′-2-ethanesulfonic acid buffer and were then adjusted to the original concentration (∼ 250 000/mL). Pooled Igs purified with protein A/G beads were adjusted to the final concentration of 10 mg/mL. (B) Platelet aggregation induced by Hp 49503 was inhibited in PRP and in washed platelets with pooled Igs where anti-CD62P antibodies applied.

Anti–P-selectin antibodies completely inhibit H pylori–induced platelet aggregation. Before the addition of H pylori (platelet/bacteria ratio = 25:1) and aggregation activators, anti-CD62P antibodies were incubated with PRP for 1 minute. (A) Addition of anti-CD62P antibodies was found to inhibit aggregations induced by pro-aggregatory Hp 49503, AA, and epinephrine. PRP, washed platelets, and pooled Igs were obtained from the anti-Hp antibody-positive samples. Washed platelets were prepared by resuspending the pellets of PRP mixture in N-2-hydroxyethylpiperazine-N′-2-ethanesulfonic acid buffer and were then adjusted to the original concentration (∼ 250 000/mL). Pooled Igs purified with protein A/G beads were adjusted to the final concentration of 10 mg/mL. (B) Platelet aggregation induced by Hp 49503 was inhibited in PRP and in washed platelets with pooled Igs where anti-CD62P antibodies applied.

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