CXCL1-Triggered Interaction of LFA1 and ICAM1 Control Glucose-Induced Leukocyte Recruitment during Inflammation In Vivo
Figure 1
Leukocyte adhesion (number of adherent cells/mm2) in mouse cremaster muscle venules and leukocyte transmigration (perivascular neutrophils/mm2 surface area) in cremaster muscle whole mounts in response to glucose during trauma-induced inflammation. (a) Leukocyte adhesion was observed in trauma-stimulated cremaster muscle venules of wild-type mice (64 venules in 16 mice), LFA1-KO mice (19–25 venules in 4 mice), and ICAM1-KO mice (18–22 venules in 4 mice) before and during 15 minutes after intravenous injection of 0.5 g/kg glucose. To dissect the role of the chemokine pathway in this model, WT mice were either pretreated with 4 μg PTx 3 h prior to cremaster exteriorization and glucose stimulation or coinjected with 600 ng CXCL1 (KC) and glucose and compared to injection of normal saline. WT mice injected with the equivalent volume of normal saline (18 venules in 4 mice) and the biologically inactive L-glucose (13–28 venules in 5 mice) served as controls. (b) Giemsa-stained cremaster muscle whole mounts of WT mice were analyzed for the number of perivascular neutrophils (per mm2 surface area) after injection of glucose or normal saline in the trauma model). In parallel, leukocyte extravasation was quantified in glucose-treated LFA1-KO, ICAM1-KO mice, and WT mice pretreated with 4 μg PTx 3 h prior to cremaster muscle exteriorization or coinjected with 600 ng CXCL1. To further illustrate the results representative micrographs of cremaster muscle whole mounts are shown in (c)–(i). Reference bar is shown in (c). Arrows point to extravasated leukocytes. All values are presented as mean ± SEM. Significances are indicated by the asterisks (* versus WT control mice).
