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High Throughput SiRNA Screening for Chloropicrin and Hydrogen Fluoride-Induced Cornea Epithelial Cell Injury
Published on: June 16, 2018
Development of mouse models for the study of chloropicrin and hydrogen fluoride ocular injury
Robert D Causey1, Jeffrey A Koenig1, Jeffrey J Autrey2
1Research Division, U.S. Army Medical Research Institute of Chemical Defense, Aberdeen Proving Ground, Harford County, Maryland.
Abstract:
The possibility of chemical terrorism within the United States is a rising concern, with the eye being one of the most sensitive tissues to toxicant exposure. We sought to develop mouse models of toxicant-induced ocular injury for the purpose of evaluating potential therapeutics. Chloropicrin (CP) and hydrogen fluoride (HF) were selected for the study owing to their reportedly high potential to induce ocular injury. Eyes of female BALB/c mice were exposed to CP or HF vapor in order to produce a moderate injury, as defined by acute corneal epithelial loss followed by progressive corneal pathology with the absence of injury to deeper eye structures. Clinical injury progression was evaluated up to 12 weeks postexposure, where a significant dose-dependent induction of corneal neovascularization was measured. Histopathology noted epithelial necrosis and stromal edema as early as 24 h after exposure but was resolved by 12 weeks. A significant increase in inflammatory cytokine concentrations was measured in the cornea 24 h after exposure and returned to baseline by day 14. The ocular injury models we developed here for CP and HF exposure should serve as a valuable tool for the future evaluation of novel therapeutics and the molecular mechanisms of injury.
Insights
Researchers developed mouse models for toxicant-induced ocular injury using chloropicrin (CP) and hydrogen fluoride (HF). These models are crucial for evaluating new therapies and understanding injury mechanisms in the eye.
Area of Science:
- Toxicology
- Ophthalmology
- Chemical Injury
Background:
- Chemical terrorism poses a significant threat, with the eye being particularly vulnerable to toxicant exposure.
- Developing reliable models for ocular injury is essential for therapeutic research.
Purpose of the Study:
- To create and characterize mouse models of toxicant-induced ocular injury.
- To evaluate the potential of chloropicrin (CP) and hydrogen fluoride (HF) in inducing controlled ocular damage.
- To establish a foundation for testing novel therapeutics and investigating injury mechanisms.
Main Methods:
- Female BALB/c mice were exposed to controlled concentrations of chloropicrin (CP) or hydrogen fluoride (HF) vapor.
- Ocular injury was assessed clinically and histopathologically up to 12 weeks post-exposure.
- Corneal neovascularization, epithelial loss, and inflammatory cytokine levels were quantified.
Main Results:
- A dose-dependent induction of corneal neovascularization was observed.
- Acute epithelial necrosis and stromal edema were noted, resolving by 12 weeks.
- Elevated corneal inflammatory cytokine concentrations peaked at 24 hours and returned to baseline by 14 days.
Conclusions:
- The developed mouse models effectively replicate moderate ocular injuries from CP and HF exposure.
- These models provide a valuable platform for evaluating therapeutic interventions for chemical-induced eye injuries.
- Further research can utilize these models to elucidate the molecular pathways involved in ocular toxicant injury.
