Increased levels of circulating ICAM-1 in serum and cerebrospinal fluid of patients with active multiple sclerosis. Correlation with TNF-alpha and blood-brain barrier damage

J Neuroimmunol. 1993 Mar;43(1-2):15-21. doi: 10.1016/0165-5728(93)90070-f.


The mechanism for the initiation of blood-brain barrier damage and intrathecal inflammation in multiple sclerosis (MS) is poorly understood. We have recently reported that levels of tumor necrosis factor-alpha (TNF-alpha) correlate with blood-brain barrier damage in patients with active MS. Stimulation of endothelial cells by TNF-alpha induces the expression of intercellular adhesion molecule-1 (ICAM-1), which is an important early marker of immune activation and response. We report herein for the first time the detection of high levels of free circulating ICAM-1 in serum and cerebrospinal fluid of patients with active MS. Levels of circulating ICAM-1 in these patients correlated with CSF pleocytosis, TNF-alpha levels and blood-brain barrier damage. These findings have important implications for the understanding and investigation of the intrathecal inflammatory response in active MS.

MeSH terms

  • Adult
  • Blood-Brain Barrier*
  • Cell Adhesion Molecules / blood*
  • Cell Adhesion Molecules / cerebrospinal fluid*
  • Cell Adhesion Molecules / physiology
  • Humans
  • Inflammation / etiology
  • Intercellular Adhesion Molecule-1
  • Multiple Sclerosis / metabolism*
  • Tumor Necrosis Factor-alpha / analysis*


  • Cell Adhesion Molecules
  • Tumor Necrosis Factor-alpha
  • Intercellular Adhesion Molecule-1