LPS-induced pulmonary neutrophil recruitment can be reconstituted with PVWT but not P1V1 or P1V3 platelets. (A) P1V1 and P1V3 platelets show reduced surface expression of PSGL1. Mice were challenged with LPS or mock-challenged as in Figure 2, and the surface expression of PSGL1 on platelets in peripheral blood was assessed after 4 hours. Data are mean ± SEM of n = 5 to 8 mice/genotype; statistics 2-way ANOVA with Bonferroni multiple comparisons test. (B) P1V1 and P1V3 platelets are not sequestered during LPS-induced acute lung inflammation. Mice were challenged with LPS as in (A) and platelet numbers in peripheral blood assessed 4 hours after challenge. Data are from 2 experiments and are mean ± SEM of n = 4 to 8 mice/genotype; statistics 2-way ANOVA with Bonferroni multiple comparisons test for genotypes. (C) P1V1 and P1V3 mice show reduced PNC formation. Mice were challenged with LPS as in (A) and the percentage of neutrophils that were attached to platelets in peripheral blood assessed 4 hours after challenge. Data are mean ± SEM of n = 6 to 8 mice/genotype; statistics 2-way ANOVA with Bonferroni multiple comparisons test. (D) Reconstitution of LPS-induced pulmonary neutrophil recruitment in platelet-depleted PVWT mice with PVWT but not P1V1 and P1V3 platelets. Isolated platelets were transfused into thrombocytopenic PVWT mice and neutrophil recruitment into LPS-inflamed lungs assessed as in Figure 2A. Data are mean ± SEM of n = 3 to 5 mice; statistics 1-way ANOVA with Bonferroni multiple comparisons. (E) Reconstitution of LPS-induced neutrophil adhesion to the airway postcapillary venule wall with PVWT but not P1V1 and P1V3 platelets. Isolated platelets were transfused into thrombocytopenic PVWT mice, lung inflammation was induced as in (A), and neutrophil adhesion to airway postcapillary venule walls was assessed by intravital microscopy 4 hours after LPS challenge as in Figure 3A. Data are mean ± SEM of n = 3 mice/group from 5 to 10 videos/animal; statistics 1-way ANOVA with Bonferroni multiple comparisons.