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NETWORK PHARMACOLOGY AND IN VITRO ANTI-S. EPIDERMIDIS EFFECTS OF QUERCETIN: COMPUTATIONAL INSIGHTS INTO IL-17 SIGNALLING AND NEUTROPHIL EXTRACELLULAR TRAPS

RAMESA SHAFI BHAT *, MONA SHUJAA ALHARBI, ABEER M. ALDBASS, SOOAD AL-DAIHAN

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Staphylococcus epidermidis can cause severe infections, particularly in immunocompromised patients, and its increasing antimicrobial resistance is a clinical concern. The mechanisms underlying the antibacterial activity of quercetin against this organism remain unclear. This study combined in vitro antibacterial assays with network pharmacology and molecular docking. Antibacterial activity was evaluated using agar well diffusion, minimum inhibitory concentration (MIC), minimum bactericidal concentration (MBC), growth-curve analysis, Fourier-transform infrared (FTIR) spectroscopy, and oxidative-stress markers in quercetin-treated S. epidermidis. Potential human host targets were identified using online prediction tools and evaluated by protein-protein interaction (PPI), Gene Ontology (GO), and Kyoto Encyclopaedia of Genes and Genomes (KEGG) enrichment analyses. Molecular docking was used to predict quercetin-target interactions. Quercetin exhibited concentration-dependent antibacterial activity against S. epidermidis, with MIC and MBC values of 125 and 500 µg/mL, respectively, sustained growth suppression, and treatment-associated FTIR changes. Network pharmacology identified 24 overlapping human host targets enriched in IL-17 signalling and neutrophil extracellular trap formation. Molecular docking predicted favourable binding affinities between quercetin and MMP1, CTSG, LCN2, CASP3, and ELANE. These computational results indicate potential associations with host immune-response pathways but do not establish immunomodulatory activity. The findings demonstrate moderate direct antibacterial activity in vitro and provide hypothesis-generating predictions of host-response mechanisms that require experimental validation.