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Amprenavir Protects Lung Epithelial Cells From Pepsin Induced Inflammation and Fibrotic Changes
Karolina Lungova1, Pelin Ergun1, Pawjai Khampang1
1Department of Otolaryngology and Communication Sciences, Medical College of Wisconsin, Milwaukee, Wisconsin, USA.
The Laryngoscope
|August 12, 2026
Summary
Amprenavir, an HIV drug, effectively reversed pepsin-induced inflammation and fibrosis in airway cells. This suggests amprenavir
Area of Science:
- Pulmonary Medicine
- Gastroenterology
- Pharmacology
Background:
- Chronic reflux-related microaspiration is a risk factor for progressive fibrotic lung diseases like IPF and CLAD.
- Gastric enzyme pepsin in nonacid reflux is a key contributor to aspiration-related lung injury.
- Previous studies indicated amprenavir reduces pepsin-mediated inflammation and fibrosis.
Purpose of the Study:
- To evaluate the time- and dose-dependent effects of pepsin on human bronchial/tracheal epithelial cells (HBECs).
- To assess the protective role of amprenavir against pepsin-induced cellular damage.
Main Methods:
- HBECs were exposed to varying concentrations and durations of pepsin (0.1 or 1 mg/mL; 15 or 30 min).
- Cells were co-treated with amprenavir (10 μM) and incubated for 6 or 24 hours.
- Pro-inflammatory markers (IL-8) and fibrotic markers (fibronectin, E-cadherin, vimentin) were measured.
Main Results:
- Low-dose pepsin increased IL-8 secretion, an effect reversed by amprenavir.
- High-dose pepsin exposure led to decreased E-cadherin and increased vimentin, both mitigated by amprenavir.
- Pepsin demonstrated dose- and time-dependent pro-inflammatory and fibrotic effects.
Conclusions:
- Pepsin exposure causes dose- and time-dependent inflammation and fibrosis in airway epithelial cells.
- Amprenavir effectively prevented these pepsin-induced cellular changes.
- Amprenavir shows therapeutic potential for mitigating airway damage from chronic reflux and progressive fibrotic lung diseases.
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