We have discovered a new mode of permeabilization of the endothelium barrier by induction of transcellular tunnels in response to a group of toxins capable of disrupting the organization of the actin cytoskeleton. This involves the transient opening within cells of tunnels of several microns in diameter that are associated with the appearance of edema and hemorrhage symptoms, as well as the dissemination of bacteria in tissues. Transient opening of tunnels is also observed during the diapedesis of immune cells through the endothelium. Our multidisciplinary studies with the physicists of the Institut Curie and the Institut Pasteur of Lille have allowed us to define that this phenomenon is similar to the so-called process of dewetting of a viscous film. In reaction to enlargement of these tunnels, the cells form a rigid actin cable, which encircles the periphery to limit their opening. Cells also produce membrane ruffles, which extend over the tunnels to close them. The dysfunction of this system of guard correlates with an induction of hemorrhage.