Figure 1
Figure 1. Role of CCR1 and CCR5 for CCL3-elicited leukocyte responses. (A) Representative RLOT in vivo microscopy images of postcapillary venules in WT, Ccr1-, and Ccr5-deficient mice after stimulation with CCL3 (scale bar: 20 μm). Leukocyte intravascular firm adherence and transmigration were quantified in postcapillary venules of the cremaster muscle as detailed in “Quantification of leukocyte kinetics and microhemodynamic parameters.” (B-C) Results for PBS-treated WT control mice as well as for WT, Ccr1-, and Ccr5-deficient mice after stimulation with CCL3 (mean ± SEM for n = 6 per group; #P < .05, vs unstimulated; *P < .05, vs WT). (D) Intravascular adherence and (E) transmigration of fluorescence-labeled bone marrow leukocytes were quantified in the cremaster muscle using in vivo fluorescence microscopy as detailed in “Quantification of florescent leukocyte responses.” Panels show results for WT mice receiving leukocytes from WT, Ccr1-, or Ccr5-deficient donors as well as for Ccr1- and Ccr5-deficient mice receiving leukocytes from WT donors after stimulation with CCL3 (mean ± SEM for n = 7 per group; #P < .05, vs unstimulated; *P < .05, vs WT→WT).

Role of CCR1 and CCR5 for CCL3-elicited leukocyte responses. (A) Representative RLOT in vivo microscopy images of postcapillary venules in WT, Ccr1-, and Ccr5-deficient mice after stimulation with CCL3 (scale bar: 20 μm). Leukocyte intravascular firm adherence and transmigration were quantified in postcapillary venules of the cremaster muscle as detailed in “Quantification of leukocyte kinetics and microhemodynamic parameters.” (B-C) Results for PBS-treated WT control mice as well as for WT, Ccr1-, and Ccr5-deficient mice after stimulation with CCL3 (mean ± SEM for n = 6 per group; #P < .05, vs unstimulated; *P < .05, vs WT). (D) Intravascular adherence and (E) transmigration of fluorescence-labeled bone marrow leukocytes were quantified in the cremaster muscle using in vivo fluorescence microscopy as detailed in “Quantification of florescent leukocyte responses.” Panels show results for WT mice receiving leukocytes from WT, Ccr1-, or Ccr5-deficient donors as well as for Ccr1- and Ccr5-deficient mice receiving leukocytes from WT donors after stimulation with CCL3 (mean ± SEM for n = 7 per group; #P < .05, vs unstimulated; *P < .05, vs WT→WT).

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