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Complement depletion affects demyelination and inflammation in experimental allergic neuritis
F J Vriesendorp1, R E Flynn, M A Pappolla
1Department of Neurology, University of Texas Health Science Center, Houston 77030, USA.
Journal of Neuroimmunology
|May 1, 1995
Summary
Complement depletion using cobra venom factor (CVF) reduced disease severity and inflammation in experimental allergic neuritis (EAN) rats. This suggests complement aids macrophage recruitment and myelin phagocytosis in EAN.
Area of Science:
- Neuroimmunology
- Complement System Biology
Background:
- Experimental allergic neuritis (EAN) is an animal model for Guillain-Barré syndrome.
- The role of the complement system in EAN pathogenesis is not fully understood.
Purpose of the Study:
- To investigate the effect of systemic complement depletion on EAN.
- To elucidate the role of complement in macrophage infiltration and myelin phagocytosis during EAN.
Main Methods:
- Rats were immunized with bovine peripheral nerve myelin to induce EAN.
- Systemic complement depletion was achieved using cobra venom factor (CVF).
- Clinical scores, demyelination, inflammation, and immune cell infiltrates (ED1, CD11bc) were assessed via immunocytochemistry.
Main Results:
- CVF treatment significantly reduced clinical scores, demyelination, and endoneurial inflammation in low-dose myelin EAN rats.
- CVF treatment decreased the number of phagocytic macrophages and CR3-expressing cells in endoneurial infiltrates.
- These effects were partially reversed when animals were immunized with a higher dose of myelin.
Conclusions:
- Complement activation plays a significant role in the pathogenesis of EAN.
- Complement may mediate macrophage recruitment into the endoneurium.
- Complement may opsonize myelin, facilitating its phagocytosis by macrophages in EAN.