Figure 8.
Figure 8. Activation-dependent integrin αIIbβ3 is not required for bacterial attachment or induction of thrombocytopenia. (A) Resting (Rest) or thrombin-activated (Act.) wild-type (+/+; ▪) or β3-integrin–deficient (–/–; □) mouse platelets were incubated with B hermsii DAH-Vsp8 in the presence or absence of 10 mM EDTA, and platelet binding was measured by flow cytometry. Shown are the means ± SDs of 2 independent experiments. **P < .001 with activated platelets from –/–mice. (B-C) 129Sv/C57BL6 wild-type (+/+; •)or β3-integrin–deficient (–/–; ○) mice were inoculated intraperitoneally with 106 B hermsii DAH or HS1. (B) At peak spirochetemia on day 2 after infection, the percentages of platelets with bound bacteria were quantified by flow cytometry (see “Materials and methods”). Shown are the means ± SDs of 8 mice from each group. (C) On the indicated days after infection, spirochete and platelet counts were determined. Shown are the means ± SDs of 10 mice from each group.

Activation-dependent integrin αIIbβ3 is not required for bacterial attachment or induction of thrombocytopenia. (A) Resting (Rest) or thrombin-activated (Act.) wild-type (+/+; ▪) or β3-integrin–deficient (–/–; □) mouse platelets were incubated with B hermsii DAH-Vsp8 in the presence or absence of 10 mM EDTA, and platelet binding was measured by flow cytometry. Shown are the means ± SDs of 2 independent experiments. **P < .001 with activated platelets from –/–mice. (B-C) 129Sv/C57BL6 wild-type (+/+; •)or β3-integrin–deficient (–/–; ○) mice were inoculated intraperitoneally with 106B hermsii DAH or HS1. (B) At peak spirochetemia on day 2 after infection, the percentages of platelets with bound bacteria were quantified by flow cytometry (see “Materials and methods”). Shown are the means ± SDs of 8 mice from each group. (C) On the indicated days after infection, spirochete and platelet counts were determined. Shown are the means ± SDs of 10 mice from each group.

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