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

https://doi.org/10.1016/0165-5728(93)90070-FGet rights and content

Abstract

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-α (TNF-α) correlate with blood-brain barrier damage in patients with active MS. Stimulation of endothelial cells by TNF-α 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-α levels and blood-brain barrier damage. These findings have important implications for the understanding and investigation of the intrathecal inflammatory response in active MS.

References (36)

  • J.W. Dawson

    The histology of disseminated sclerosis

    Trans. R. Soc. Edinb.

    (1916)
  • M.S. Diamond et al.

    ICAM-1 (CD54): a counter-receptor for Mac-1 (CD11a/CD18)

    J. Cell. Biol.

    (1990)
  • D. Gay et al.

    Blood-brain barrier damage in acute multiple sclerosis plaques. An immunocytological study

    Brain

    (1991)
  • C.P. Hawkins et al.

    Patterns of blood-brain barrier breakdown in inflammatory demyelination

    Brain

    (1991)
  • Y. Ishii et al.

    Tumor necrosis factor-α-mediated decrease in glutathione increases the sensitivity of pulmonary vascular endothelial cells to H2O2

    J. Clin. Invest.

    (1992)
  • H. Lassmann et al.

    Expression of adhesion molecules and histocompatibility antigens at the blood-brain barrier

    Brain Pathol.

    (1991)
  • S.K. Lo et al.

    Tumor necrosis factor mediates experimental pulmonary edema by ICAM-1 and CD18-dependent mechanisms

    J. Clin. Invest.

    (1992)
  • C.E. Lumsden

    The neuropathology of multiple sclerosis

  • Cited by (192)

    • Multiple Sclerosis

      2016, International Encyclopedia of Public Health
    • Treatment with tanshinone IIA suppresses disruption of the blood-brain barrier and reduces expression of adhesion molecules and chemokines in experimental autoimmune encephalomyelitis

      2016, European Journal of Pharmacology
      Citation Excerpt :

      Vascular cell adhesion protein-1 (VCAM-1) mediates the capture of pathogenic CD4+ T cells on the BBB endothelium and intercellular cell adhesion molecule-1 (ICAM-1) arrests T cells on the BBB and assists with T cell diapedesis across the BBB. ICAM-1 and VCAM-1 have long been implicated in the pathogenesis of MS. In active MS and EAE lesions, ICAM-1 and VCAM-1 on endothelial cells, astrocytes and microglial cells show diffuse overexpression and increased activity (Lee and Benveniste, 1999; Carrithers et al., 2000; Sharief et al., 1993; Rieckmann et al., 1993). ICAM1−/− mice show attenuated EAE, with markedly reduced T cell infiltration in the spinal cord (Bullard et al., 2007).

    View all citing articles on Scopus
    View full text