Fig. 2.
Fig. 2. G-CSF and IL-17 levels are elevated in leukocyte adhesion molecule–deficient mice. / Severely neutrophilic CD18−/− mice showed significantly elevated levels of (A) G-CSF and (D) IL-17 compared with wild-type mice (P < .05). G-CSF and IL-17 levels in E−/−(open circles), EP−/− (closed squares), EPI−/− (open squares), CD18−/− (open triangles), CD18−/−E−/− (closed triangles), and CD18−/−P−/− (open diamonds) mice were elevated in proportion to the level of neutrophilia in these mice (B,E). C57BL/6 wild-type mice are indicated by closed circles. Data are expressed as mean ± SEM (n = 4-14). Elevated (C) G-CSF and (F) IL-17 levels in individual leukocyte adhesion molecule–deficient mice correlated with circulating neutrophil levels (r = 0.73 and r = 0.62, respectively). The correlation between G-CSF or IL-17 levels and neutrophil counts regardless of genotype suggests a common mechanism of altered hematopoiesis resulting from impaired leukocyte trafficking.

G-CSF and IL-17 levels are elevated in leukocyte adhesion molecule–deficient mice.

Severely neutrophilic CD18−/− mice showed significantly elevated levels of (A) G-CSF and (D) IL-17 compared with wild-type mice (P < .05). G-CSF and IL-17 levels in E−/−(open circles), EP−/− (closed squares), EPI−/− (open squares), CD18−/− (open triangles), CD18−/−E−/− (closed triangles), and CD18−/−P−/− (open diamonds) mice were elevated in proportion to the level of neutrophilia in these mice (B,E). C57BL/6 wild-type mice are indicated by closed circles. Data are expressed as mean ± SEM (n = 4-14). Elevated (C) G-CSF and (F) IL-17 levels in individual leukocyte adhesion molecule–deficient mice correlated with circulating neutrophil levels (r = 0.73 and r = 0.62, respectively). The correlation between G-CSF or IL-17 levels and neutrophil counts regardless of genotype suggests a common mechanism of altered hematopoiesis resulting from impaired leukocyte trafficking.

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