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NSAID-induced antral ulcers are associated with distinct changes in mucosal gene expression
1Department of Medicine (Division of Gastroenterology), The Mount Sinai Medical Center, New York, NY, USA.
Alimentary Pharmacology & Therapeutics
|March 25, 2009
Summary
Nonsteroidal anti-inflammatory drug (NSAID)-induced ulcers are linked to specific gene expression patterns in the gastroduodenal mucosa. This research may explain individual differences in NSAID susceptibility.
Area of Science:
- Gastroenterology
- Molecular Biology
- Pharmacology
Background:
- Individual susceptibility to NSAID-induced gastroduodenal damage varies.
- The underlying molecular mechanisms for this variation are not fully understood.
Purpose of the Study:
- To investigate if a specific gene expression signature correlates with susceptibility to NSAID-induced gastroduodenal ulcers.
- To identify potential biomarkers for predicting ulcer development.
Main Methods:
- Twenty-five NSAID-naive individuals received naproxen for seven days.
- Endoscopic biopsies were collected pre- and post-treatment for gene expression analysis of 23 relevant genes.
- Gene expression fold changes were compared between ulcer and non-ulcer groups.
Main Results:
- Individuals developing antral ulcers showed significantly higher mucosal upregulation of interleukin-8 and cyclo-oxygenase-2 compared to non-ulcer subjects.
- Conversely, non-ulcer subjects exhibited greater upregulation of toll-like receptor-4, cyclo-oxygenase-1, and hepatocyte growth factor.
Conclusions:
- A distinct gastroduodenal mucosal gene expression profile is associated with NSAID-induced antral ulcers.
- These findings offer insights into the molecular basis of individual susceptibility to NSAID-induced mucosal injury.
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