In vitro correlates of endothelial injury and repair.
The effects of immune complexes, microbial components, and glomerular basement membrane on cultured human umbilical endothelial cells were assessed in vitro using phase contrast microscopy, cell counts, 51Cr release, and terminal tritiated thymidine-labeling assays. Neither heat-aggregated IgG nor bovine serum albumin-antibovine serum albumin immune complexes altered endothelial cell growth as measured by cell counts, thymidine labeling, and phase contrast microscopy, nor did immune complexes induce cytotoxicity as measured by 51Cr release. Some microbial components appeared cytotoxic to endothelial cells, other microbial components had no effect, and one, clostridial neuraminidase, induced proliferation of endothelial cells as measured by phase contrast microscopy, cell counts, and thymidine labeling. Native and glycosidase-altered glomerular basement membrane also enhanced endothelial cell thymidine labeling. These studies show that microbial components directly alter endothelial cell growth in vitro, whereas immune complexes by themselves do not. Thus, in vivo microbial components by themselves may directly affect endothelial cells and cause vascular pathology, whereas immune complexes presumably must recruit other inflammatory systems to affect endothelial cells. Alterations of basement membrane during inflammation may also affect endothelial growth and, thus, vascular pathology.
D000936:Antigen-Antibody Complex; D001485:Basement Membrane / Q000502:physiology; D002455:Cell Division; D002478:Cells, Cultured; D003602:Cytotoxicity, Immunologic; D004261:DNA Replication; D004727:Endothelium / Q000166:cytology / Q000276:immunology / Q000502:physiology*; D005260:Female; D006801:Humans; D007074:Immunoglobulin G; D007678:Kidney Glomerulus / Q000502:physiology; D011247:Pregnancy; D013291:Streptococcus / Q000276:immunology; D014471:Umbilical Veins; D014945:Wound Healing
D000936:Antigen-Antibody Complex; D007074:Immunoglobulin G