Permeability Changes in the Human Endothelial Cell Line, SGHEC-7, Caused by IL-1β, TNFα and Substance P

Abstract

Vascular microvessels normally have low permeability to macromolecules. During an inflammatory reaction, however, this barrier function is lost and fluid leaks from the vessel into the tissues. Soluble mediators, such as cytokines an vasoactive hormones are thought to contribute to this process. Recent technical advances in endothelial cell (EC) culture and the production of porous membranes have allowed the study of EC permeability in vitro (Albelda et al., 1988; Burke-Gaffney and Keenan, 1993). Permeability of EC monolayer grown on porous membranes has been shown to increase following stimulation with recombinant human interleukin-1α(rHuIL-1α) and -β and recombinant human tumor necrosis factor-α(rHuTNFα) (Burke-Gaffney and Keenan, 1993). In vivo substance P dilates human arterial and venous beds in skeletal muscle (McEwan et al., 1988) and skin (Foreman et al., 1983). Substance P has also been shown to dilate isolated human large vessels where the responses seem to be endothelium dependent in arteries (Luscher and Vanhoutte, 1988) but not in all veins (Luu et al., 1992) and may contribute to oedema formation by increasing vascular permeability.