Soluble complement receptor 1 (sCR1) is not as effective as Cobra Venom Factor in the treatment of Experimental Allergic Neuritis

Francine J. Vriesendorp, Robyn E. Flynn, Miguel Pappolla, Carol L. Koski

Research output: Contribution to journalArticle

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Abstract

To further investigate the role of complement activation in Experimental Allergic Neuritis (FAN), the effect of systemic complement blockade by soluble CR1 (sCR1) was compared to complement depletion by Cobra Venom Factor (CVF) in EAN rats immunized with bovine peripheral nerve myelin. EAN rats treated with CVF (n = 10) had significantly reduced clinical scores compared to rats treated with sCR1 (n = 9) or saline (n = 10)(score: sCR1 0.66 ± 0.7; CVF 0; saline 0.6 ± 0.8; mean ± SD). CVF treatment more effectively decreased inflammation and demyelination compared to sCR1 treatment which had only a partial effect (inflammation: sCR1 1.8 ± 1.4; CVF 0.3 ± 0.7; saline 1.9 ± 1.2; demyelination; sCR1 1.3 ± 1; CVF 0.1 ± 0.6; saline 1.7 ± 1.2). In lumbosacral nerve roots significantly less infiltrating ED1 positive macrophages and CD1 1bc (expressing complement receptor 3 or CR3) positive inflammatory cells were present in CVF treated EAN rats while there was a limited decrease in inflammation in the sCR1 treated animals compared to the saline treated rats (ED1: sCR1 1.4 ± 1.2; CVF 0.5 ± 0.6; saline 1.7 ± 1.2; CD1 1bc: sCR1 1.9 ± 1.2; CVF 0.9 ±1 ; saline 2.1 ± 1.2). Our findings suggest that complement depletion by CVF is more effective than complement blockade by sCR1 in reducing the severity of inflammatory peripheral nerve demyelination.

Original languageEnglish (US)
Pages (from-to)287-298
Number of pages12
JournalInternational Journal of Neuroscience
Volume92
Issue number3-4
StatePublished - Dec 1997
Externally publishedYes

Fingerprint

Experimental Autoimmune Neuritis
Complement C1
Complement Receptors
Demyelinating Diseases
Inflammation
Peripheral Nerves
cobra venom factor
Macrophage-1 Antigen
Complement Activation
Myelin Sheath

Keywords

  • Complement
  • Demyelination
  • EAN
  • Macrophage
  • Soluble Complement Receptor 1

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Soluble complement receptor 1 (sCR1) is not as effective as Cobra Venom Factor in the treatment of Experimental Allergic Neuritis. / Vriesendorp, Francine J.; Flynn, Robyn E.; Pappolla, Miguel; Koski, Carol L.

In: International Journal of Neuroscience, Vol. 92, No. 3-4, 12.1997, p. 287-298.

Research output: Contribution to journalArticle

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abstract = "To further investigate the role of complement activation in Experimental Allergic Neuritis (FAN), the effect of systemic complement blockade by soluble CR1 (sCR1) was compared to complement depletion by Cobra Venom Factor (CVF) in EAN rats immunized with bovine peripheral nerve myelin. EAN rats treated with CVF (n = 10) had significantly reduced clinical scores compared to rats treated with sCR1 (n = 9) or saline (n = 10)(score: sCR1 0.66 ± 0.7; CVF 0; saline 0.6 ± 0.8; mean ± SD). CVF treatment more effectively decreased inflammation and demyelination compared to sCR1 treatment which had only a partial effect (inflammation: sCR1 1.8 ± 1.4; CVF 0.3 ± 0.7; saline 1.9 ± 1.2; demyelination; sCR1 1.3 ± 1; CVF 0.1 ± 0.6; saline 1.7 ± 1.2). In lumbosacral nerve roots significantly less infiltrating ED1 positive macrophages and CD1 1bc (expressing complement receptor 3 or CR3) positive inflammatory cells were present in CVF treated EAN rats while there was a limited decrease in inflammation in the sCR1 treated animals compared to the saline treated rats (ED1: sCR1 1.4 ± 1.2; CVF 0.5 ± 0.6; saline 1.7 ± 1.2; CD1 1bc: sCR1 1.9 ± 1.2; CVF 0.9 ±1 ; saline 2.1 ± 1.2). Our findings suggest that complement depletion by CVF is more effective than complement blockade by sCR1 in reducing the severity of inflammatory peripheral nerve demyelination.",
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