Molecular mechanisms of baicalein in treating recalcitrant chronic rhinosinusitis Caused by Staphylococcus aureus.
Molecular mechanisms of baicalein in treating recalcitrant chronic rhinosinusitis Caused by Staphylococcus aureus: An in vitro study.
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Abstract
BACKGROUND/PURPOSE(S): Staphylococcus aureus overgrowth contributes to chronic rhinosinusitis (CRS) through biofilm formation, bacterial invasion, and immune evasion. These factors lead to persistent infections and complications, especially in cases of refractory CRS. This study examines baicalein's effects on bacterial virulence and host responses using Calu-3 cells as an in vitro testing platform. METHODS: Baicalein's effects on S. aureus-induced epithelial damage were evaluated in a Calu-3 cell co-culture model. The analyses included bacterial clumping, biofilm formation, internalization, tight junction integrity, oxidative stress, apoptosis, and key signaling pathways. RESULTS: Baicalein inhibited bacterial clumping, biofilm formation, and internalization by downregulating key virulence genes (fnbpA, fnbpB, clfB, rot, sarA, and icaR). It also suppressed the Agr and LuxS/AI-2 quorum sensing systems, which regulate virulence and biofilm development. In host cells, baicalein reduced S. aureus-induced apoptosis by modulating the PI3K/Akt pathway and attenuated oxidative stress and autophagy. Furthermore, it restored epithelial barrier integrity by preserving ZO-1 localization. CONCLUSION: Baicalein demonstrates potential as an alternative therapeutic strategy for reducing CRS recurrence and minimizing prolonged antibiotic use by effectively targeting S. aureus virulence and disrupting bacterial communication. This approach offers a promising solution for managing CRS and reducing reliance on antibiotics.
Affiliation
Chung-Ching Lin
External References
- PubMed ID:
- 40441980
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