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S100B immunization triggers NFκB and complement activation in an autoimmune glaucoma model.

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Glaucoma involves the complement system. Mannose-binding lectin (MBL) activation and NFκB increase in retinas suggest a pathway for glaucomatous damage, even without elevated eye pressure.

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Area of Science:

  • Ophthalmology
  • Immunology
  • Neuroscience

Background:

  • Glaucoma pathogenesis is increasingly linked to complement system activation, independent of intraocular pressure.
  • The S100B protein is implicated in experimental autoimmune glaucoma models, causing retinal ganglion cell (RGC) loss and optic nerve damage.

Purpose of the Study:

  • To investigate the temporal progression of the complement system, toll-like receptor 4 (TLR4), and nuclear factor-kappa B (NFκB) in an S100B-induced experimental autoimmune glaucoma model.
  • To elucidate the role of the lectin pathway in complement activation and subsequent RGC and optic nerve damage.

Main Methods:

  • Rats were immunized with S100B protein and analyzed at 3, 7, and 14 days post-immunization.
  • Quantification of RGCs, optic nerve degeneration, and analysis of complement components (MBL, C3), IL-1β, TLR4, and NFκB activation in retinal and optic nerve tissues.

Main Results:

  • Optic nerve degeneration was observed by day 14, while RGC numbers remained comparable across time points.
  • Mannose-binding lectin (MBL) levels increased in retinas by day 3 and in optic nerves by days 7 and 14.
  • Complement component C3 and interleukin-1 beta were upregulated, and NFκB activation was significantly increased in retinas at 7 and 14 days. No changes in TLR4 were noted.

Conclusions:

  • Complement activation via the MBL-dependent lectin pathway is evident in this glaucoma model.
  • NFκB activation, potentially triggered by MBL, may contribute to glaucomatous damage.
  • These findings highlight a complement-mediated pathway in glaucoma pathogenesis, offering potential therapeutic targets.