A monokine regulates colony-stimulating activity production by vascular endothelial cells.
Human umbilical vein endothelial cells were cultured in supernatants of peripheral blood monocytes that had been cultured for 3 days with and without lactoferrin. Colony-stimulating activity (CSA) was measured in supernatants of the endothelial cell cultures and appropriate control cultures using normal, T-lymphocyte-depleted, phagocyte-depleted, low-density bone marrow cells in colony growth (CFU-GM) assays. Monocyte-conditioned medium contained a nondialyzable, heat labile factor that enhanced 4-15--fold the production of CSA by endothelial cells. The addition of lactoferrin to monocyte cultures reduced the activity of this monokine by 69%. Lactoferrin did not inhibit CSA production by monokine-stimulated endothelial cells. Therefore, vascular endothelial cells are potent sources of CSA, the production of CSA by these cells is regulated by a stimulatory monokine, and the production and/or release of the monokine is inhibited by lactoferrin, a neutrophil-derived putative feedback inhibitor of granulopoiesis. Inasmuch as a similar monokine is known to stimulate CSA production by fibroblasts and T lymphocytes, we suggest that mononuclear phagocytes play a pivotal role in the regulation of granulopoiesis by recruiting a variety of cell types to produce CSA.
D002478:Cells, Cultured; D003115:Colony-Stimulating Factors / Q000096:biosynthesis*; D004727:Endothelium / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D006801:Humans; D007781:Lactoferrin / Q000494:pharmacology; D015846:Monokines; D011506:Proteins / Q000494:pharmacology*; D014471:Umbilical Veins / Q000187:drug effects / Q000378:metabolism*
D003115:Colony-Stimulating Factors; D015846:Monokines; D011506:Proteins; D007781:Lactoferrin