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Systemic complement depletion reduces inflammation and demyelination in adoptive transfer experimental allergic
F J Vriesendorp1, R E Flynn, M R Malone
1Department of Neurology, University of Texas Health Science Center, Houston 77030, USA. fvriesen@neuro.med.uth.tmc.edu
Acta Neuropathologica
|May 30, 1998
Summary
Systemic complement depletion using cobra venom factor (CVF) significantly reduced inflammation and demyelination in experimental allergic neuritis (EAN). This approach also decreased macrophage infiltration in nerve tissues, highlighting complement's role in EAN pathogenesis.
Area of Science:
- Neuroimmunology
- Inflammatory Demyelination
- Complement System Biology
Background:
- Experimental Allergic Neuritis (EAN) is an autoimmune model of inflammatory demyelination.
- The role of the complement system in EAN pathogenesis is not fully understood.
- Adoptive transfer EAN (AT-EAN) provides a model to study specific immune mechanisms.
Purpose of the Study:
- To investigate the effect of systemic complement depletion on AT-EAN.
- To determine if complement plays a role in inflammatory cell recruitment and demyelination in AT-EAN.
- To assess the impact of complement depletion on macrophage infiltration in nerve tissues.
Main Methods:
- Adoptive transfer of spleen cells from SP26-immunized rats to naive rats to induce AT-EAN.
- Systemic complement depletion using cobra venom factor (CVF) or saline treatment on days 3 and 6 post-transfer.
- Histological scoring of nerve root inflammation and demyelination.
- Immunocytochemical analysis for ED1-positive macrophages and CD11bc-positive inflammatory cells.
Main Results:
- CVF-treated AT-EAN rats showed significantly lower histological scores for inflammation (P < 0.03) and demyelination (P < 0.02) compared to saline-treated controls.
- Immunocytochemistry revealed significantly reduced numbers of ED1-positive macrophages (P < 0.04) and CD11bc-positive cells (P < 0.03) in the nerve roots of CVF-treated rats.
- These findings indicate that complement depletion curtails the infiltration of macrophages and inflammatory cells.
Conclusions:
- Complement plays a critical role in the inflammatory demyelination observed in AT-EAN.
- Systemic complement depletion effectively reduces macrophage recruitment into the nerve.
- Complement activation is essential for subsequent macrophage-mediated demyelination in this EAN model.