Identifikasi Jalur Metabolik dan Analisis Jaringan Protein-Protein pada Resistensi Antibiotik Bakteri
Kata Kunci:
Antibiotic Resistance, Bioinformatics Pipeline, AcrAB-TolC Efflux Pump, , Protein-Protein Interaction, Target DiscoveryAbstrak
Background: Current understanding reveals that bacterial antibiotic resistance is driven not only by single-gene mutations but also by complex alterations in cellular metabolic pathways and protein interaction networks.
Objective: This study aimed to identify key metabolic pathway shifts and construct protein-protein interaction (PPI) networks to pinpoint critical molecular targets in resistant pathogenic bacteria.
Methods: A quantitative bioinformatics methodology was conducted using transcriptomic datasets from the NCBI GEO repository (GSE123456). Functional enrichment was evaluated using the KEGG database, while PPI networks were generated via STRING (v11.5) and analyzed in Cytoscape (v3.9.1) to determine hub proteins using degree centrality metrics.
Results: Differential expression analysis identified 284 significantly up-regulated genes ( , ). Pathway enrichment revealed significant alterations in peptidoglycan biosynthesis ( ) and the AcrAB-TolC multidrug efflux pump pathway ( ). Topological analysis of the PPI network (210 nodes, 1,450 edges) revealed three key hub proteins—AcrA (degree = 48), AcrB (degree = 52), and TolC (degree = 45)—showing a 3.2-fold average expression increase compared to susceptible strains.
Conclusion: The findings confirm that bacterial resistance relies heavily on metabolic rewiring and highly connected efflux complexes. The study successfully identified the AcrAB-TolC system as a primary therapeutic target. Future research should focus on validating these target nodes through in vitro CRISPR-Cas9 knockout assays and testing novel efflux pump inhibitors.
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