Fig. 5.
Fig. 5. Effect of anti-α4-integrins monoclonal antibody (mAb) (TA-2) and anti–VCAM-1 mAb (5F10) on eosinophil recruitment into rat skin and pleural cavities. / (A) In the experiments with rat skin, 4 groups of rats were given intravenous injections of saline, control mouse IgG (3.5 mg/kg), TA-2 (3.5 mg/kg), or 5F10 (3.5 mg/kg). Fifteen minutes later, the animals were injected intradermally with RPMI (100 μL/site) or IL-4 (5000 units/100 μL per site). Eosinophil accumulation in the skin sites, as quantified by measurement of EPO activity, was determined 24 hours after injection. Because there were no differences between EPO levels in RPMI-injected sites among the 4 different groups tested, these data were pooled (■). Results are expressed as the mean ± SEM value for 3 to 15 pairs of rats. A significant difference (P < .01) from levels in RPMI-treated rats is indicated by one asterisk. Also, significant differences (P < .05) between responses in animals given the control antibody and those given the anti-α4-integrins mAb or the anti–VCAM-1 mAb are indicated by + symbols. (B) The same groups of rats were also used in an experiment in which the animals received intrapleural IL-4 (5000 units/100 μL per cavity) or RPMI (100 μL) 15 minutes after the intravenous injections described above. Eosinophil accumulation in the pleural cavity was determined 24 hours later. The results are expressed as the mean ± SEM value for 6 to 8 animals per group. A significant difference (P < .01) from levels in RPMI-treated rats is indicated by one asterisk. Significant differences (P < .05) between responses in animals given the control antibody and those given the anti-α4-integrins mAb or the anti–VCAM-1 mAb are indicated by + symbols. Data were analyzed with a one-way analysis of variance followed by a Newman-Keuls comparison test.

Effect of anti-α4-integrins monoclonal antibody (mAb) (TA-2) and anti–VCAM-1 mAb (5F10) on eosinophil recruitment into rat skin and pleural cavities.

(A) In the experiments with rat skin, 4 groups of rats were given intravenous injections of saline, control mouse IgG (3.5 mg/kg), TA-2 (3.5 mg/kg), or 5F10 (3.5 mg/kg). Fifteen minutes later, the animals were injected intradermally with RPMI (100 μL/site) or IL-4 (5000 units/100 μL per site). Eosinophil accumulation in the skin sites, as quantified by measurement of EPO activity, was determined 24 hours after injection. Because there were no differences between EPO levels in RPMI-injected sites among the 4 different groups tested, these data were pooled (■). Results are expressed as the mean ± SEM value for 3 to 15 pairs of rats. A significant difference (P < .01) from levels in RPMI-treated rats is indicated by one asterisk. Also, significant differences (P < .05) between responses in animals given the control antibody and those given the anti-α4-integrins mAb or the anti–VCAM-1 mAb are indicated by + symbols. (B) The same groups of rats were also used in an experiment in which the animals received intrapleural IL-4 (5000 units/100 μL per cavity) or RPMI (100 μL) 15 minutes after the intravenous injections described above. Eosinophil accumulation in the pleural cavity was determined 24 hours later. The results are expressed as the mean ± SEM value for 6 to 8 animals per group. A significant difference (P < .01) from levels in RPMI-treated rats is indicated by one asterisk. Significant differences (P < .05) between responses in animals given the control antibody and those given the anti-α4-integrins mAb or the anti–VCAM-1 mAb are indicated by + symbols. Data were analyzed with a one-way analysis of variance followed by a Newman-Keuls comparison test.

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