Fig. 5.
Fig. 5. VCAM-1 and 4-integrins participate in eosinophil accumulation and tethering to IL-4–stimulated HUVECs. Monolayers of HUVECs were treated as described in Fig 1. Before assembly of the flow chamber, HUVECs were treated for 10 minutes at 37°C with HBSS/A alone or HBSS/A containing 5 μg/mL of 1.G11B1, an MoAb directed against VCAM-1. Alternatively, eosinophils were pretreated 10 minutes at 37°C with 2 μg/mL of H2/1, an anti–4-integrin MoAb, before perfusion over IL-4–stimulated HUVECs. The flow chamber was assembled and eosinophils also containing the specified MoAb were perfused through the chamber. (A) Tethering of eosinophils was determined at 2 dyn/cm2, as described in Materials and Methods. (B) Accumulation of eosinophils was determined at the specified wall shear stresses as described in Materials and Methods. The data represent the mean and SEM of at least three independent experiments. *P ≤ .05; **P ≤ .0001.

VCAM-1 and 4-integrins participate in eosinophil accumulation and tethering to IL-4–stimulated HUVECs. Monolayers of HUVECs were treated as described in Fig 1. Before assembly of the flow chamber, HUVECs were treated for 10 minutes at 37°C with HBSS/A alone or HBSS/A containing 5 μg/mL of 1.G11B1, an MoAb directed against VCAM-1. Alternatively, eosinophils were pretreated 10 minutes at 37°C with 2 μg/mL of H2/1, an anti–4-integrin MoAb, before perfusion over IL-4–stimulated HUVECs. The flow chamber was assembled and eosinophils also containing the specified MoAb were perfused through the chamber. (A) Tethering of eosinophils was determined at 2 dyn/cm2, as described in Materials and Methods. (B) Accumulation of eosinophils was determined at the specified wall shear stresses as described in Materials and Methods. The data represent the mean and SEM of at least three independent experiments. *P ≤ .05; **P ≤ .0001.

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