Endothelial adhesiveness for blood neutrophils is inhibited by transforming growth factor-beta.
Adhesion of blood cells to endothelial cells is an essential component of all inflammatory responses. The capacity of the endothelium to support adhesion of neutrophils is increased by cytokines such as tumor necrosis factor-alpha, interleukin-1, and endotoxin. Another cytokine, transforming growth factor-beta (TGF-beta), was a strong inhibitor of basalneutrophil adhesion and also decreased the adhesive response of endothelial cells to tumor necrosis factor-alpha (TNF-alpha). The ability of cells to respond to TGF-beta was related to the duration of culture of endothelial cells after explantation from umbilical veins. TGF-beta is likely to serve an anti-inflammatory role at sites of blood vessel injury undergoing active endothelial regeneration.
Gamble
J R
JR
Division of Human Immunology, Institute of Medical and Veterinary Science, Adelaide, South Australia.
Vadas
M A
MA
D002448:Cell Adhesion / Q000187:drug effects; D002478:Cells, Cultured; D004730:Endothelium, Vascular / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D006801:Humans; D007700:Kinetics; D009504:Neutrophils / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D015291:Transforming Growth Factors / Q000494:pharmacology*; D014471:Umbilical Veins
D015291:Transforming Growth Factors