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Author Spotlight: Investigating the Pathophysiology of Eosinophilic Esophagitis
Published on: May 10, 2024
921
Mitochondrial dysfunction drives basal cell hyperplasia in eosinophilic oesophagitis
Masaki Morimoto1, Kento Kawasaki1, Niamh McNamee2
1Columbia University Herbert Irving Comprehensive Cancer Center, New York, New York, USA.
Gut
|July 23, 2025
Summary
Mitochondrial dysfunction drives basal cell hyperplasia in eosinophilic esophagitis (EoE). Omeprazole treatment improved mitochondrial health and reduced hyperplasia in EoE models, suggesting a therapeutic role.
Area of Science:
- Gastroenterology
- Immunology
- Cell Biology
Background:
- Eosinophilic esophagitis (EoE) is an IL-13-mediated inflammatory disorder of the esophagus.
- The role of mitochondria in EoE pathogenesis is not well understood.
Purpose of the Study:
- To investigate the role of mitochondria in EoE pathobiology.
- To determine if omeprazole affects mitochondrial function in EoE.
Main Methods:
- Utilized patient biopsies, mouse models, and 3D organoid cultures.
- Performed CRISPR interference to identify key mitochondrial regulatory genes.
- Analyzed mitochondrial function, cellular respiration, and energy homeostasis.
Main Results:
- Mitochondrial dysfunction, including structural damage and impaired ATP production, was a hallmark of EoE-related basal cell hyperplasia (BCH).
- Depletion of PGC1A, a mitochondrial biogenesis regulator, mimicked EoE-related BCH.
- Omeprazole treatment ameliorated mitochondrial damage and dysfunction in EoE models.
Conclusions:
- Mitochondrial dysfunction and redox imbalance are linked in EoE-related BCH.
- IL-13 promotes BCH, which can be reversed by omeprazole treatment.
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