Effects of lipopolysaccharide on endothelial cell adhesion molecule expression in interleukin-10 deficient mice

Inflammation. 1999 Apr;23(2):99-110. doi: 10.1023/a:1020232826906.


Interleukin (IL)-10 is known to inhibit the production of proinflammatory cytokines by macrophages suggesting that endogenous IL-10 may act as an antiinflammatory agent. Because endothelial cell adhesion molecules (ECAMs) play a key role in the recruitment of leukocytes into tissue in response to an inflammatory stimulus (i.e., lipopolysaccharide (LPS)) and the following cytokine production, we wished to assess the importance of IL-10 as an endogenous modulator of ECAM expression using IL-10 deficient mice. Constitutive and LPS-stimulated expression of intercellular adhesion molecule (ICAM)-1, vascular cell adhesion molecule (VCAM)-1 and E-selectin were measured in wild type C57BL/6 and IL-10 deficient mice with no signs of active enterocolitis, using the dual radiolabeled monoclonal antibody technique. We found that constitutive expression of these ECAMs did not differ between IL-10 deficient and WT mice for all organs tested. However, we demonstrated larger increments in LPS-induced expression of ICAM-1 and VCAM-1 in the vasculature of the small intestine in IL-10 deficient mice compared to WT mice. These findings suggest that endogenous IL-10 does not modulate constitutive or LPS-induced expression of ECAMs in most tissues, however it does appear to play an inhibitory role in LPS-stimulated expression of ICAM-1 and VCAM-1 in the intestinal vasculature.

Publication types

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

MeSH terms

  • Animals
  • Antibodies, Monoclonal / metabolism
  • Down-Regulation
  • Endothelium, Vascular / chemistry
  • Endothelium, Vascular / drug effects*
  • Inflammation Mediators / physiology
  • Intercellular Adhesion Molecule-1 / analysis
  • Interleukin-10 / deficiency*
  • Interleukin-10 / physiology
  • Lipopolysaccharides / pharmacology*
  • Mice
  • Mice, Inbred BALB C
  • Mice, Mutant Strains
  • Platelet Endothelial Cell Adhesion Molecule-1 / analysis
  • Platelet Endothelial Cell Adhesion Molecule-1 / biosynthesis*
  • Random Allocation
  • Tumor Necrosis Factor-alpha / metabolism
  • Vascular Cell Adhesion Molecule-1 / analysis


  • Antibodies, Monoclonal
  • Inflammation Mediators
  • Lipopolysaccharides
  • Platelet Endothelial Cell Adhesion Molecule-1
  • Tumor Necrosis Factor-alpha
  • Vascular Cell Adhesion Molecule-1
  • Intercellular Adhesion Molecule-1
  • Interleukin-10