Figure 4.
Figure 4. CD44, but not RHAMM, mediates neutrophil adhesion to HA in sinusoids, but not postsinusoidal venules. The numbers of (A) rolling and (B) adherent neutrophils were counted per 100 μm in postsinusoidal venules, and (C) the number of adherent leukocytes in sinusoidal capillaries was determined by intravital microscopy. (D) Leder-stained liver sections were viewed by standard light microscopy, and positively stained neutrophils were counted per hpf (×400) of view. For all parameters, LPS-treated WT (wt, black bar), LPS-treated CD44 knockout (CD44−/−), LPS-treated WT mice injected with anti-CD44 mAb (anti-CD44 mAb), and LPS-treated WT mice receiving anti-RHAMM mAb were compared with untreated WT mice (wt, white bar). Data are presented as arithmetic mean ± SEM of at least five animals per group. *, P < 0.05 relative to untreated controls; #, P < 0.05 relative to LPS-treated WT animals.

CD44, but not RHAMM, mediates neutrophil adhesion to HA in sinusoids, but not postsinusoidal venules. The numbers of (A) rolling and (B) adherent neutrophils were counted per 100 μm in postsinusoidal venules, and (C) the number of adherent leukocytes in sinusoidal capillaries was determined by intravital microscopy. (D) Leder-stained liver sections were viewed by standard light microscopy, and positively stained neutrophils were counted per hpf (×400) of view. For all parameters, LPS-treated WT (wt, black bar), LPS-treated CD44 knockout (CD44−/−), LPS-treated WT mice injected with anti-CD44 mAb (anti-CD44 mAb), and LPS-treated WT mice receiving anti-RHAMM mAb were compared with untreated WT mice (wt, white bar). Data are presented as arithmetic mean ± SEM of at least five animals per group. *, P < 0.05 relative to untreated controls; #, P < 0.05 relative to LPS-treated WT animals.

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