# Cord Blood Serum Attenuates Hyperosmolarity-Induced Inflammation and TRPV1 Upregulation in Conjunctival Epithelial Cells

## TL;DR

Cord Blood Serum reduces inflammation and pain in eye cells stressed by high salt levels, suggesting it could be a useful treatment for eye surface diseases.

## Contribution

This study demonstrates that Cord Blood Serum can downregulate inflammation and TRPV1 in hyperosmotic conditions, offering a novel bioactive tear substitute.

## Key findings

- CBS improves cell viability in hyperosmotic stress.
- CBS reduces HLA-DR and TRPV1 expression in stressed cells.
- Neurotrophins are likely involved in CBS's protective effects.

## Abstract

Eye drops derived from human blood components (Eye Drops of Human Origin—EDHO) have proven effective in reducing ocular pain associated with severe keratopathies. Among these, Cord Blood Serum (CBS) is particularly promising for its high content of growth and neurotrophic factors. This study evaluated the ability of CBS to modulate inflammatory and nociceptive activation in the human conjunctival epithelial cell (HCEC) line exposed to hyperosmotic stress. CBS batches were characterized for brain-derived neurotrophic factor (BDNF) content and classified as CBShigh (levels > 18.0 ng/mL) or CBSlow (levels < 10.0 ng/mL). HCECs were exposed to NaCl (450 mOsm/L) with or without 5% CBS. Cell viability was evaluated, and the expression of Major Histocompatibility Complex Class II (HLA-DR) (a marker of immune activation) and Transient Receptor Potential Vanilloid 1 (TRPV1) (a nociceptive ion channel responsive to osmotic stress) was assessed via Real Time PCR (RT-PCR). CBS significantly improved HCEC viability under hyperosmotic stress. Exposure to NaCl alone upregulated HLA-DR and TRPV-1 expression. Both CBS preparations attenuated these responses, producing comparable reductions in HLA-DR mRNA and decreasing TRPV-1 expression. Partial reversal of CBS effects by the pan-neurotrophin receptor inhibitor K252a supported neurotrophin involvement. CBS reduces hyperosmolarity-driven inflammation and nociception via HLA-DR and TRPV1 downregulation, supporting its role as a bioactive tear substitute in neuroinflammatory ocular surface disease.