Fig. 8.
Fig. 8. Stimulation with β1-activating mAb 8A2 results in stable arrest of rolling eosinophils in IL-1β–stimulated mesenteric venules. / Eosinophils were incubated ex vivo with anti-β1 integrin–activating mAb 8A2 (20 μg/mL) for 3 to 5 minutes prior to administration of eosinophils into the rabbit mesentery. The ability of the rolling eosinophils to adhere firmly in postcapillary venules (treated with anti-VCAM-1 mAb Rb 1/9 or control antibody (IgG1) (as described in Figure 7) was determined. The results represent the number of adherent eosinophils per 250 μm length of venule (mean ± SD) during the 5 minutes of eosinophil infusion after resumption of blood flow. Eosinophil control vs eosinophil and β1-activating mAb 8A2 (P = .02); eosinophil and β1-activating mAb 8A2 vs anti-VCAM-1 mAb Rb 1/9 (P = .04): anti-VCAM-1 vs mouse IgG1 control (P = .05).

Stimulation with β1-activating mAb 8A2 results in stable arrest of rolling eosinophils in IL-1β–stimulated mesenteric venules.

Eosinophils were incubated ex vivo with anti-β1 integrin–activating mAb 8A2 (20 μg/mL) for 3 to 5 minutes prior to administration of eosinophils into the rabbit mesentery. The ability of the rolling eosinophils to adhere firmly in postcapillary venules (treated with anti-VCAM-1 mAb Rb 1/9 or control antibody (IgG1) (as described in Figure 7) was determined. The results represent the number of adherent eosinophils per 250 μm length of venule (mean ± SD) during the 5 minutes of eosinophil infusion after resumption of blood flow. Eosinophil control vs eosinophil and β1-activating mAb 8A2 (P = .02); eosinophil and β1-activating mAb 8A2 vs anti-VCAM-1 mAb Rb 1/9 (P = .04): anti-VCAM-1 vs mouse IgG1 control (P = .05).

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