Systemic complement depletion reduces inflammation and demyelination in adoptive transfer experimental allergic neuritis

Francine J. Vriesendorp, Robyn E. Flynn, Michael R. Malone, Miguel A. Pappolla

Research output: Contribution to journalArticle

20 Scopus citations

Abstract

The effect of systemic complement depletion by cobra venom factor (CVF) was evaluated in adoptive transfer experimental allergic neuritis (AT-EAN). Spleen cells of rats immunized with a neuritogenic peptide SP26 were injected into naive rats. On days 3 and 6 after cell transfer AT-EAN rats were treated with CVF or saline intraperitoneally. AT-EAN rats treated with CVF had significantly lower scores for histological inflammation (0.25 ± 0.25 vs 1.9 ± 0.4, mean ± SEM, P < 0.03) and demyelination (0.13 ± 0.13 vs 1.6 ± 1.4, P < 0.02) than saline-treated AT-EAN rats. Immunocytochemistry of lumbosacral nerve roots showed significantly less ED1-positive macrophages (0.5 ± 0.3 vs 1.6 ± 0.6, P < 0.04) and CD11bc-positive (expressing complement receptor 3 or CR3) inflammatory cells (0.6 ± 0.4 vs 1.7 ± 0.5, P < 0.03). Our data suggest that complement plays a crucial role in inflammatory demyelination since systemic complement depletion significantly reduces recruitment of macrophages into the nerve and subsequent macrophage-mediated demyelination.

Original languageEnglish (US)
Pages (from-to)297-301
Number of pages5
JournalActa Neuropathologica
Volume95
Issue number3
DOIs
StatePublished - Mar 30 1998
Externally publishedYes

Keywords

  • Adoptive transfer experimental allergic neuritis
  • Complement
  • Demyelination
  • Inflammation
  • Macrophage

ASJC Scopus subject areas

  • Pathology and Forensic Medicine
  • Clinical Neurology
  • Cellular and Molecular Neuroscience

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