Anti-Intercellular Adhesion Molecule-1 (ICAM-1) antibody treatment prevents central and peripheral nervous system disease in autoimmune-prone mice

R. L. Brey, A. A. Amato, K. Kagan-Hallet, C. B. Rhine, Christian Stallworth

Research output: Contribution to journalArticlepeer-review

26 Scopus citations

Abstract

Abnormal neurological functioning similar to that seen in systemic lupus erythematosus (SLE) patients is detectable in an SLE-prone murine strain (MRL/1pr) by 8-10 weeks and is severe by 18 weeks of age. The purpose of this study was to evaluate the effectiveness of murine anti-intercellular adhesion molecule-1 (ICAM-1) in suppressing neurological disease in MRL/1pr mice. Beginning at 6 weeks of age, five MRL/1pr mice received 5 weekly intraperitoneal injections of anti-ICAM-1-containing culture supernatant in phosphate-buffered saline (PBS) whereas four animals were treated with non-anti-ICAM-1 containing supernatant in PBS. A decline in neurological functioning began in control mice by 10 weeks, but anti-ICAM-1 treated mice remained normal throughout the study. All control mice had vasculitic skin lesions by 14 weeks of age whereas none of the anti-ICAM-1 treated mice ever developed skin lesions. Nerve conduction studies performed on all mice prior to sacrifice showed sciatic compound motor action potentials of anti-ICAM-1 treated mice that were of higher amplitude and shorter latency than those of controls. Inflammation in the sciatic nerve was more common in control mice. Brain histology revealed a similar degree of choroid plexus inflammation in both groups. Our study demonstrated that anti-ICAM-1 was effective in suppressing neurological abnormalities in MRL/1pr mice and may potentially be useful therapy in human SLE.

Original languageEnglish (US)
Pages (from-to)645-651
Number of pages7
JournalLupus
Volume6
Issue number8
DOIs
StatePublished - 1997

Keywords

  • Intercellular adhesion molecule-1
  • MRL/1pr mice
  • Nerve conduction studies
  • Systemic lupus erythematosus

ASJC Scopus subject areas

  • Rheumatology

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