Monokine-induced gene expression of a human endothelial cell-derived neutrophil chemotactic factor.
Monokines have been increasingly recognized as communication signals that interact with both immune and non-immune cells during inflammation. Specifically, interleukin-1 alpha (IL-1 alpha), interleukin-1 beta (IL-1 beta) and tumor necrosis factor-alpha (TNF-alpha) possess potent effector activities on various cell types. We present novel data demonstrating that human endothelial cells are a major source of a neutrophil chemotactic factor (NCF) synthesized upon stimulation with either IL-1 alpha, IL-1 beta, or TNF-alpha; but not with interleukin-6 (IL-6). Northern blot analysis demonstrated that 20 ng/ml of either IL-1 or TNF-alpha could induce endothelial cells to express significant levels of NCF mRNA, while IL-6 was not active in this system. These data demonstrate that monokines play an important role in mediating acute inflammation via induction of an endothelial cell-derived NCF.
Strieter
R M
RM
Department of Internal Medicine, University of Michigan Medical School, Ann Arbor.
Kunkel
S L
SL
Showell
H J
HJ
Marks
R M
RM
D001345:Autoradiography; D001685:Biological Factors / Q000494:pharmacology*; D002630:Chemotactic Factors / Q000235:genetics*; D002634:Chemotaxis, Leukocyte / Q000187:drug effects; D003720:Densitometry; D004730:Endothelium, Vascular / Q000032:analysis / Q000187:drug effects*; D005786:Gene Expression Regulation / Q000187:drug effects*; D007375:Interleukin-1 / Q000494:pharmacology; D015846:Monokines; D009504:Neutrophils / Q000276:immunology; D012333:RNA, Messenger / Q000032:analysis; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology
D001685:Biological Factors; D002630:Chemotactic Factors; D007375:Interleukin-1; D015846:Monokines; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha