Membrane interleukin 1 induction on human endothelial cells and dermal fibroblasts

J Immunol. 1987 Oct 1;139(7):2317-24.

Abstract

Human endothelial cells and dermal fibroblasts both expressed a membrane-associated interleukin 1 (IL-1) activity when stimulated with either recombinant tumor necrosis factor (TNF) or recombinant lymphotoxin but stimulated endothelial cells expressed significantly more membrane IL-1 per cell than did fibroblasts. Lipopolysaccharide induced membrane IL-1 activity on endothelial cells but not fibroblasts. Interferon-gamma treatment of endothelial cells and fibroblasts had no direct effect on membrane IL-1 expression and little effect when used as a pretreatment for TNF or lipopolysaccharide stimulation. Endothelial cell membrane IL-1 activity was induced within 24 hr of culture with TNF or lipopolysaccharide, and increased up to 72 hr of incubation. Antibodies raised against human monocyte-derived IL-1 species neutralized the membrane IL-1 activity of TNF-stimulated endothelial cells. Both absorption studies and neutralization with specific sera indicated that endothelial cell membrane IL-1 is structurally related to IL-1 alpha. Endothelial cells expressed both IL-1 beta mRNA in response to TNF, lymphotoxin, and recombinant IL-1 species, as detected by Northern blot analysis. These studies demonstrate that endothelial cells can be activated to express a cell-surface IL-1 activity which is structurally, as well as functionally, related to the secreted form of IL-1.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Cell Membrane / analysis
  • Endothelium, Vascular / cytology
  • Endothelium, Vascular / drug effects*
  • Endothelium, Vascular / metabolism
  • Fibroblasts / cytology
  • Fibroblasts / drug effects*
  • Fibroblasts / metabolism
  • Gene Expression Regulation / drug effects
  • Humans
  • Interferon-gamma / pharmacology
  • Interleukin-1 / biosynthesis*
  • Lipopolysaccharides / pharmacology*
  • Lymphotoxin-alpha / pharmacology*
  • Membrane Proteins / biosynthesis*
  • Recombinant Proteins / pharmacology
  • Skin / cytology
  • Stimulation, Chemical
  • Tumor Necrosis Factor-alpha / pharmacology*

Substances

  • Interleukin-1
  • Lipopolysaccharides
  • Lymphotoxin-alpha
  • Membrane Proteins
  • Recombinant Proteins
  • Tumor Necrosis Factor-alpha
  • Interferon-gamma