Figure 3
Figure 3. Altered neutrophil rolling and impaired adhesion in airway postcapillary venules of P1V1 and P1V3 mice during acute LPS-induced lung inflammation. (A) Altered neutrophil rolling and impaired adhesion in airway postcapillary venules of P1V1 and P1V3 mice during LPS-induced lung inflammation. Mice were challenged with LPS as in Figure 3 and intravital microscopy was performed by taking 15-second videos of 5 to 10 of the airway postcapillary venules/mouse. Numbers of rolling neutrophils (i), rolling velocity (ii; mean velocity and speed categories), and firm adhesion (iii) were assessed by video analysis. Data are mean ± SEM of 4 to 5 mice/group for numbers of rolling and adhering cells. Rolling velocity is median speed of ≥90 cells/genotype; statistics unpaired Student t test between sham- and LPS-treatment or Kruskal-Wallis test with Dunn’s multiple comparisons for genotypes. (B) Representative images of LPS-induced neutrophil recruitment in airway postcapillary venules. Inflammation was induced with LPS and was monitored by airway intravital microscopy as in (A). Images are stills from representative videos. White arrows denote firmly adhering neutrophils (stationary throughout recording), and black arrows show cells rolling along the vessel wall. (C) Neutrophil-intrinsic and neutrophil-extrinsic factors are sufficient to impair LPS-induced pulmonary neutrophil recruitment in P1V3 mice. Mice were lethally irradiated, their hematopoietic system was reconstituted with bone marrow, as indicated, LPS-dependent lung inflammation was induced after reconstitution, and pulmonary neutrophil recruitment was assessed by intravital microscopy as in (A). Data are mean ± SEM of 4 to 5 mice/group; statistics as in (A).

Altered neutrophil rolling and impaired adhesion in airway postcapillary venules of P1V1 and P1V3 mice during acute LPS-induced lung inflammation. (A) Altered neutrophil rolling and impaired adhesion in airway postcapillary venules of P1V1 and P1V3 mice during LPS-induced lung inflammation. Mice were challenged with LPS as in Figure 3 and intravital microscopy was performed by taking 15-second videos of 5 to 10 of the airway postcapillary venules/mouse. Numbers of rolling neutrophils (i), rolling velocity (ii; mean velocity and speed categories), and firm adhesion (iii) were assessed by video analysis. Data are mean ± SEM of 4 to 5 mice/group for numbers of rolling and adhering cells. Rolling velocity is median speed of ≥90 cells/genotype; statistics unpaired Student t test between sham- and LPS-treatment or Kruskal-Wallis test with Dunn’s multiple comparisons for genotypes. (B) Representative images of LPS-induced neutrophil recruitment in airway postcapillary venules. Inflammation was induced with LPS and was monitored by airway intravital microscopy as in (A). Images are stills from representative videos. White arrows denote firmly adhering neutrophils (stationary throughout recording), and black arrows show cells rolling along the vessel wall. (C) Neutrophil-intrinsic and neutrophil-extrinsic factors are sufficient to impair LPS-induced pulmonary neutrophil recruitment in P1V3 mice. Mice were lethally irradiated, their hematopoietic system was reconstituted with bone marrow, as indicated, LPS-dependent lung inflammation was induced after reconstitution, and pulmonary neutrophil recruitment was assessed by intravital microscopy as in (A). Data are mean ± SEM of 4 to 5 mice/group; statistics as in (A).

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