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Differences in vascular permeability between normal tissue and a tumor. Vascular permeability, often in the form of capillary permeability or microvascular permeability, characterizes the capacity of a blood vessel wall to allow for the flow of small molecules (drugs, nutrients, water, ions) or even whole cells (lymphocytes on their way to the site of inflammation) in and out of the vessel.
However, the endothelial barrier is subjected to damage as a result of viral infection. Therapeutics that enhance or regain the integrity endothelial barrier after it has been damaged have been considered as potential targets for emerging infectious diseases like COVID-19, Ebola, Dengue fever, and more.
Excessive or prolonged increases in permeability of the endothelium, as in cases of chronic inflammation, may lead to tissue swelling . Altered barrier function is also implicated in cancer extravasation. [6] Endothelial cells are involved in many other aspects of vessel function, including: Blood clotting (thrombosis and fibrinolysis).
The permeability of a capillary wall is determined by the type of capillary and the surface of the endothelial cells. A continuous, tightly spaced endothelial cell lining only permits the diffusion of small molecules. Larger molecules and blood cells require adequate space between cells or holes in the lining.
For example, the apical surface of gastrointestinal epithelial cells serve as a selective permeable barrier that separates the external environment from the body. [3] The permeability of these junctions is dependent on a variety of factors including protein makeup of that junction, tissue type and signaling from the cells.
Diffusion through the capillary walls depends on the permeability of the endothelial cells forming the capillary walls, which may be continuous, discontinuous, and fenestrated. [4] The Starling equation describes the roles of hydrostatic and osmotic pressures (the so-called Starling forces ) in the movement of fluid across capillary endothelium .
Skin immunity is a property of skin that allows it to resist infections from pathogens. In addition to providing a passive physical barrier against infection, the skin also contains elements of the innate and adaptive immune systems which allows it to actively fight infections. Hence the skin provides defense in depth against infection.
TP0965 causes endothelial barrier dysfunction, a hallmark of late-stage pathogenesis of syphilis. [34] It does this by reducing the expression of tight junction proteins, which in turn increases the expression of adhesion molecules and endothelial cell permeability, which eventually leads to disruption of the endothelial layer. [35]