Ocular surface epithelia express mRNA for human beta defensin-2

Area of Science:

• Immunology
• Ophthalmology
• Microbiology

Background:

• Human beta-defensin-2 (hBD-2) is an antibiotic peptide found in skin, lung, and trachea, contributing to infection resistance.
• The corneal epithelium's resistance to infection suggests a potential role for antimicrobial peptides like hBD-2.

Purpose of the Study:

• To investigate whether human ocular surface epithelia produce hBD-2.
• To determine if bacterial by-products, specifically lipopolysaccharide (LPS), can upregulate hBD-2 mRNA expression in corneal epithelial cells.

Main Methods:

• Reverse transcription-polymerase chain reaction (RT-PCR) was used to detect hBD-2 mRNA in human conjunctival and corneal epithelial cells.
• SV 40-immortalized human corneal epithelial cells were stimulated with wild-type Pseudomonas aeruginosa (P. aeruginosa) culture supernatant and LPS mutants.
• LPS was extracted and used to confirm its role in hBD-2 upregulation; genistein was used to investigate the involvement of protein tyrosine kinase activity.

Main Results:

• hBD-2 mRNA was detected in both human corneal and conjunctival epithelial cells.
• Stimulation with wild-type P. aeruginosa supernatant significantly upregulated hBD-2 mRNA expression.
• LPS was identified as the causative agent for hBD-2 upregulation, with the lipid A portion not being required; protein tyrosine kinase activity appears involved.

Conclusions:

• Human corneal and conjunctival epithelia express hBD-2 mRNA.
• Bacterial LPS upregulates hBD-2 expression in these cells, independent of the lipid A component.
• Stimulating endogenous hBD-2 production via LPS may offer therapeutic strategies for ocular infections.