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Inflammatory mediators in alkali-burned corneas: preliminary characterization
S A Elgebaly1, R T Downes, M Bohr
1Vision Immunology Center, University of Connecticut School of Medicine, Farmington 06032.
Current Eye Research
|November 1, 1987
Summary
Alkali-burned corneas produce leukocyte chemotactic factors (LCF) that recruit immune cells. Citric acid significantly inhibits this LCF production, offering a potential therapeutic target for eye inflammation.
Area of Science:
- Ophthalmology
- Immunology
- Biochemistry
Background:
- Leukocyte chemotactic factors (LCF) mediate inflammation by recruiting leukocytes to damaged tissues.
- LCF have been detected in tears from alkali-burned eyes, but their origin (corneal tissue vs. circulation) is unclear.
Purpose of the Study:
- To investigate the capability of corneal tissues to produce LCF following alkali injury.
- To evaluate the effect of citric acid on LCF production in alkali-injured corneas.
Main Methods:
- Bovine and human corneas were exposed to 1N sodium hydroxide (NaOH) and incubated.
- Corneal injury and LCF production were assessed using checkerboard analysis.
- LCF biochemical properties were characterized, and the effect of citric acid was tested.
Main Results:
- NaOH induced significant corneal epithelial injury.
- Injured corneas produced significant neutrophil and mononuclear cell chemotactic activity.
- LCF were protease/heat sensitive, solvent-extractable, and >100,000 daltons.
- Citric acid markedly inhibited LCF production (91-98%).
Conclusions:
- Alkali-burned corneas generate endogenous LCF distinct from known low-molecular-weight factors.
- Citric acid effectively inhibits alkali-induced corneal LCF production.