Concomitant gut dysbiosis and defective gut barrier serve as the bridges between hypercortisolism and chronic systemic inflammation in Cushing’s disease
Authors' conclusion
Disease activity associated dysbiosis and defective gut barrier might jointly facilitate the development of systemic inflammation in patients with CD.
Study context
- Population
- Patients with Cushing's disease (CD) and healthy controls
- Participants
- 27 vs 45
- Comparison
- CD vs healthy controls
- CDn = 27
- Healthy controlsn = 45reference
- Outcome
- Gut microbial signatures and gut barrier
Methodological detailscase-control metagenomics, fecal metabolomics, in vitro Caco-2 cell experiments
- Case-control metagenomics
- Fecal metabolomics
- In vitro Caco-2 cell experiments
Main finding
As reported in the abstract
- Gut microbial composition in CD notably different from healthy controls
- Network analysis: Eubacterium siraeum might be the core species in CD gut microbiota
- Positive correlations between GIG9 and UFC
- CD patients with elevated UFC had increased lipopolysaccharide binding protein (LBP)
- Remarkable positive association between LBP and relative abundance of E. siraeum
- Hypercortisolism induced increased gut permeability (transepithelial electrical resistance (TEER), FITC-dextran assays)
- Dysregulated AhR/Claudin 2 axis might be involved in hypercortisolism-induced defective gut barrier
Original publication
Concomitant gut dysbiosis and defective gut barrier serve as the bridges between hypercortisolism and chronic systemic inflammation in Cushing’s disease. Eur J Endocrinol. Published 26 October 2024. doi:10.
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