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Preservation of optic nerve structure by complement inhibition in experimental glaucoma
Caroline J Gassel1, Sabrina Reinehr1, Sara C Gomes1
1Experimental Eye Research Institute, University Eye Hospital, Ruhr-University Bochum, In der Schornau 23-25, 44892, Bochum, Germany.
Cell and Tissue Research
|July 18, 2020
Summary
Complement factor C5 inhibition prevented optic nerve damage in an experimental autoimmune glaucoma model. This suggests complement inhibition may be a novel therapeutic strategy for glaucoma.
Area of Science:
- Ophthalmology
- Immunology
- Neuroscience
Background:
- Glaucoma involves progressive retinal and optic nerve damage, with unknown exact pathomechanisms.
- An experimental autoimmune glaucoma model in rats involves immunization with optic nerve antigen (ONA), leading to glaucoma-like damage.
- Early complement system activation precedes optic nerve degeneration in this model.
Purpose of the Study:
- To investigate the therapeutic potential of a monoclonal antibody against complement factor C5 in preventing optic nerve damage.
- To evaluate the effects of C5 inhibition on complement deposition, cellular infiltration, neurofilament preservation, and microglia activation in an autoimmune glaucoma model.
Main Methods:
- Rats were immunized with ONA to induce experimental autoimmune glaucoma.
- Intravitreal injections of a monoclonal antibody against C5 were administered to ONA-immunized rats.
- Optic nerves were analyzed histologically after 6 weeks to assess complement deposition, cellular infiltration, neurofilament integrity (SMI-32 staining), and microglia presence.
Main Results:
- Intravitreal C5 antibody therapy significantly reduced membrane attack complex deposition in optic nerves.
- Cellular infiltration was significantly reduced in one treatment group (ONA + C5-I).
- Neurofilament preservation was observed in both C5-treated groups compared to controls, and microglia levels were decreased.
Conclusions:
- Complement system inhibition, specifically targeting C5, demonstrated a protective effect against optic nerve damage in an autoimmune glaucoma model.
- These findings highlight complement inhibition as a potential novel therapeutic approach for managing glaucoma.
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