What the study found
The study found that intestinal epithelial cells and the mucosal barrier were disrupted during experimental autoimmune encephalomyelitis (EAE), a mouse model of multiple sclerosis. This disruption was linked to inhibition of mitochondrial oxidative phosphorylation (OXPHOS), the process cells use to make energy in mitochondria.
Why the authors say this matters
The authors conclude that their findings help explain a potential mechanism by which gut microbiota dysbiosis, an imbalance in gut microbes, observed in EAE mice compromises intestinal epithelial integrity and disrupts the mucosal barrier. They present this as relevant to understanding the underlying mechanisms of multiple sclerosis development.
What the researchers tested
The researchers used a multi-omics approach, combining proteomic analysis and metabolomic analysis, during EAE induction. They examined small intestinal epithelial cells and cecal contents from EAE mice to look for changes in OXPHOS-related proteins and metabolites.
What worked and what didn't
Proteomic analysis showed altered OXPHOS complexes, with a pronounced decrease in cytochrome c oxidase and ATP synthase subunits in small intestinal epithelial cells. Metabolomic analysis showed enrichment of phenyllactic acid, a phenolic acid typically produced by Lactobacillus murinus, in cecal contents, and the study reports that phenyllactic acid downregulated OXPHOS complexes and restrained maximal mitochondrial respiration.
What to keep in mind
The available summary does not describe limitations in detail. The findings are reported in experimental autoimmune encephalomyelitis mice, so the abstract does not state whether the same mechanism was directly shown in humans.
Key points
- Intestinal epithelial cells and the mucosal barrier were disrupted during EAE induction.
- The disruption was linked to inhibition of mitochondrial oxidative phosphorylation.
- Cytochrome c oxidase and ATP synthase subunits were reduced in small intestinal epithelial cells.
- Phenyllactic acid was enriched in cecal contents of EAE mice.
- The study reports that phenyllactic acid downregulated OXPHOS complexes and limited maximal mitochondrial respiration.
Disclosure
- Research title:
- Gut metabolite linked to OXPHOS-related epithelial damage in EAE
- Authors:
- Eunike Tiffany, Panida Sittipo, Chanyoung Lee, Ju Yeon Lee, Soojin Lee, Yun Kyung Lee
- Institutions:
- Burapha University, Chungnam National University, Korea Basic Science Institute, Soonchunhyang University, Soonchunhyang University, Soonchunhyang University, Soonchunhyang University
- Publication date:
- 2026-02-26
- OpenAlex record:
- View
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