Figure 7.

Volociximab and ATN-161 reduce spike-induced stimulation of EC leukocyte adhesion and permeability.A, binding of 100 nM spike or spike receptor–binding domain (RBD) to immobilized integrin α5β1 in the absence (−) or the presence of the RGD tripeptide or the integrin α5β1 inhibitors, volociximab (5 μg ml⁻¹) and ATN-161 (500 nM). B, leukocyte adhesion to HUVEC incubated without (−) or with 1 nM TNF⍺ or 100 nM spike, RBD, or RGD, in the absence or the presence of volociximab (5 μg ml⁻¹) or ATN-161 (500 nM). #p < 0.001 versus the unstimulated control (−), ∗p < 0.001 versus the absence of integrin α5β1 inhibitors (two-way ANOVA, Tukey test). C, changes throughout time of the transendothelial electrical resistance (ΔTEER) of HUVEC monolayers incubated without (−) or with 100 nM spike in the presence or the absence of volociximab (5 μg ml⁻¹) or ATN-161 (500 nM). ΔTEER values of HUVEC incubated only with volociximab or ATN-161 are also shown. Values are means ± SD, n = 6. EC, endothelial cell; HUVEC, human umbilical vein endothelial cell; RGD, arginine–glycine–aspartic acid; TNF⍺, tumor necrosis factor alpha.