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Cortisol biosynthesis in the human ocular surface innate immune response
Radhika Susarla1, Lei Liu1, Elizabeth A Walker2
1Academic Unit of Ophthalmology, Centre for Translational Inflammation Research, College of Medical and Dental Sciences, University of Birmingham, Birmingham, United Kingdom.
Plos One
|April 17, 2014
Summary
Cortisol production in corneal cells, independent of Toll-like receptor activation, aids ocular surface defense. Its role varies with disease type, impacting innate immunity and inflammation management.
Area of Science:
- Ophthalmology
- Immunology
- Cell Biology
Background:
- Ocular surface (OcS) inflammation is critical in sight-threatening conditions.
- Glucocorticoids (GCs) are used to manage tissue damage.
- The role of intracrine cortisol bioavailability via 11-beta-hydroxysteroid dehydrogenase type 1 (11β-HSD1) in OcS defense is unclear.
Purpose of the Study:
- To investigate the role of 11β-HSD1 and cortisol bioavailability in ocular surface innate immunity.
- To determine the impact of Toll-like receptor (TLR) activation on cortisol production in corneal cells.
- To analyze the relationship between local cortisol levels and specific ocular surface diseases.
Main Methods:
- Primary human corneal epithelial cells (PHCEC) and fibroblasts (PHKF) were cultured.
- Macrophage (M1, M2) differentiation and function were assessed.
- Cortisol production, 11β-HSD1 activity, and cytokine/chemokine release were measured.
- TLR agonists (PolyI:C, LPS) and GCs were used.
- Tear film cortisol:cortisone ratios were analyzed in patients with pseudomonas keratitis and TLR3-mediated diseases.
Main Results:
- Corneal cells and macrophages produce cortisol, with M1 macrophages and PHKF showing higher levels.
- Cortisol production in corneal cells was independent of TLR activation.
- PolyI:C stimulated cytokine/chemokine release from PHCEC and PHKF; GCs inhibited PHKF responses.
- Corneal cell challenge with PolyI:C or LPS induced M1 chemotaxis but reduced M1 11β-HSD1 activity.
- Tear film cortisol:cortisone ratios were reduced in pseudomonas keratitis and elevated in TLR3-mediated OcS diseases.
Conclusions:
- Cortisol biosynthesis in human corneal cells, independent of TLR activation, likely provides immunoprotection.
- The contribution of cortisol to ocular mucosal innate responses depends on the specific immunological challenge.
- 11β-HSD1 activity and local cortisol levels are altered in distinct ocular surface inflammatory conditions.
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