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Helicobacter pylori cell envelope and enzymes represent a collective group of bacterial targets essential for the survival and pathogenicity of H. pylori in the human stomach [1]. The cell envelope serves as a protective barrier and a platform for adhesion to gastric epithelial cells, while enzymes like urease allow the bacterium to survive the acidic environment by producing ammonia [1, 3]. Bismuth subsalicylate acts as a multi-target antimicrobial agent that interacts with these components to eradicate the infection [2]. It binds to the bacterial cell wall, leading to structural disruption and eventual cell lysis [3]. Furthermore, bismuth ions inhibit the activity of urease and other metabolic enzymes, effectively starving the bacteria and making them susceptible to gastric acid [1, 3]. This target complex is a cornerstone of bismuth-based quadruple therapy, which is used to treat peptic ulcers and prevent gastric cancer [4]. Because bismuth targets multiple pathways, it remains effective even against strains that have developed resistance to conventional antibiotics [4].
Bismuth subsalicylate exerts bactericidal effects by disrupting the bacterial cell wall, inhibiting the urease enzyme to prevent acid neutralization, and interfering with bacterial adhesion and protein synthesis [1, 3].
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