A Novel Target for Faster Wound Closure in Ocular Trauma
Abstract
Ocular trauma (one of the most common forms of battlefield injury) is a major cause of delayed wound closure, uncontrolled ocular inflammation, and new vessel growth, which can compromise corneal clarity. Additionally, millions of patients in the U.S. suffer each year from various ocular damages, for which there are currently limited therapeutic options that are both safe and effective. The current line of treatment is limited to pain management and non-specific anti-inflammatory drugs such as corticosteroids. However, these non-specific treatment strategies not only target tissue-damaging but also beneficial regulatory inflammation, causing side-effects such as infection, cataract, and glaucoma. Thus, there is a pressing need for a targeted therapeutic strategy that not only inhibits tissue-damaging immune cells and new blood vessel growth, but also promotes tissue repair in ocular injury. Interleukin-36 gamma, an inflammatory factor, was observed in high levels at the injured mouse ocular surface. In our preliminary study, we demonstrate that blockade of interleukin-36 gamma accelerates wound closure in a setup mimicking the human cornea. The aim of this project is to evaluate the therapeutic outcome, including rapid wound closure and suppressed ocular inflammation with reduced blood vessel growth, of blocking this inflammatory factor in damaged ocular tissue. This will provide a strong basis for the development of novel therapeutic strategies for safer and more effective treatments for ocular injuries.
Document Details
- Document Type
- DoD Grant Award
- Publication Date
- Mar 10, 2021
- Source ID
- W81XWH2010822
Entities
People
- Sunil K Chauhan
Organizations
- Schepens Eye Research Institute
- United States Army