Molecular mechanisms of baicalein in treating recalcitrant chronic rhinosinusitis Caused by Staphylococcus aureus: An...

Area of Science:

• Microbiology
• Pharmacology
• Immunology

Background:

• Staphylococcus aureus overgrowth and biofilm formation are key contributors to chronic rhinosinusitis (CRS).
• Bacterial invasion and immune evasion by S. aureus lead to persistent infections and complications, particularly in refractory CRS.
• Current treatments often involve prolonged antibiotic use, highlighting the need for alternative therapeutic strategies.

Purpose of the Study:

• To investigate the effects of baicalein on Staphylococcus aureus virulence and host responses in an in vitro model of CRS.
• To evaluate baicalein's impact on bacterial clumping, biofilm formation, and invasion.
• To assess baicalein's influence on host cell integrity, oxidative stress, apoptosis, and relevant signaling pathways.

Main Methods:

• Utilized a Calu-3 cell co-culture model to simulate S. aureus infection.
• Assessed bacterial clumping, biofilm formation, and internalization.
• Analyzed tight junction integrity, oxidative stress, apoptosis, and key signaling pathways (PI3K/Akt, autophagy).

Main Results:

• Baicalein inhibited S. aureus clumping, biofilm formation, and internalization by downregulating virulence genes (fnbpA, fnbpB, clfB, rot, sarA, icaR).
• Baicalein suppressed quorum sensing systems (Agr, LuxS/AI-2), crucial for virulence and biofilm development.
• Baicalein reduced S. aureus-induced apoptosis, attenuated oxidative stress and autophagy, and restored epithelial barrier integrity by preserving ZO-1 localization.

Conclusions:

• Baicalein shows promise as an alternative therapeutic agent for CRS by targeting S. aureus virulence and communication.
• This approach may reduce CRS recurrence and minimize the need for prolonged antibiotic treatment.
• Baicalein offers a potential strategy for managing CRS and decreasing antibiotic dependence.