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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

Tumor necrosis factor and interleukin 1 alpha increase vascular endothelial permeability.

Endotoxic shock is associated with acute vascular endothelial injury resulting in edema. Tumor necrosis factor ( TNF) and interleukin 1 (IL-1) are cytokines produced by endotoxin-stimulated mononuclear phagocytes that are potential mediators of endotoxic shock. In this study, we investigated the effects of TNF and IL-1 alpha on vascular endothelial cell permeability in vitro. The movement of radiolabeled macromolecules of different sizes (57Co-vitamin B12, 125I-cytochrome c, and 131I-albumin; 6.5-35A) across bovine aortic endothelial cell monolayers was measured after exposure to these cytokines. TNF induced a time- and dose-dependent increase in endothelial cell monolayer permeability that was enhanced in the presence of serum. The peak increase was noted after 12 h of incubation with less alteration of permeability with longer incubations. IL-1 alpha caused a similar time-dependent increase in endothelial cell monolayer permeability, but the peak effect of IL-1 alpha was seen after 24 h. Therefore the increased permeability seen with TNF cannot be explained by release of endogenous IL-1 alone. Neither TNF nor IL-1 alpha increased release of [14C]adenine, and the only effect on lactate dehydrogenase release was a small, but statistically significant, increase after 24 h of incubation. From these studies, we conclude that TNF and IL-1 alpha directly increase vascular endothelial cell permeability in vitro and speculate that these cytokines may be involved in the acute vascular endothelial injury associated with endotoxic shock.[1]

References

  1. Tumor necrosis factor and interleukin 1 alpha increase vascular endothelial permeability. Royall, J.A., Berkow, R.L., Beckman, J.S., Cunningham, M.K., Matalon, S., Freeman, B.A. Am. J. Physiol. (1989) [Pubmed]
 
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