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Experimental Autoimmune Uveitis: An Intraocular Inflammatory Mouse Model
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Comparative Proteomic Analysis of Two Uveitis Models in Lewis Rats
Investigative Ophthalmology & Visual Science
|January 10, 2016
Summary
Inflammation alters aqueous humor proteins. Proinflammatory S100A8/S100A9 increase in uveitis, while neuroprotective beta-B2-crystallin decreases in EAU, suggesting therapeutic targets.
Area of Science:
- Ophthalmology
- Immunology
- Proteomics
Background:
- Ocular inflammation, such as uveitis, significantly alters the protein composition of aqueous humor.
- Identifying specific protein changes can reveal disease biomarkers and therapeutic targets for uveitis.
Purpose of the Study:
- To identify differentially-expressed proteins in the aqueous humor of rats during experimental autoimmune uveitis (EAU) and primed mycobacterial uveitis (PMU).
Main Methods:
- Two rat models of uveitis (EAU and PMU) were established.
- Differential gel electrophoresis and MALDI-TOF mass spectrometry were used to analyze aqueous humor proteins.
- Western blot analysis confirmed the expression of select proteins in aqueous and vitreous humor.
Main Results:
- Total protein concentration increased in inflamed aqueous humor from both uveitis models.
- Calprotectin (S100A8/S100A9) was elevated in the aqueous humor in both EAU and PMU.
- Apolipoprotein E increased in both models, while beta-B2-crystallin decreased specifically in EAU.
Conclusions:
- S100A8 and S100A9 are key proinflammatory molecules in uveitis, potentially more critical in PMU.
- The decline of neuroprotective beta-B2-crystallin in EAU highlights its potential role in disease pathogenesis.
- Modulating these identified proteins presents a promising therapeutic strategy for ocular inflammation.
