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The Helicobacter pylori biofilm extracellular matrix (ECM) is a complex, self-produced assembly of extracellular polymeric substances (EPS) including polysaccharides, proteins, lipids, and extracellular DNA (eDNA) that encases the bacteria (Hathroubi et al., 2018). This matrix serves as a physical and chemical barrier, protecting H. pylori from the harsh acidic environment of the stomach, host immune defenses, and the penetration of antimicrobial agents (Yonezawa et al., 2015). Biofilm formation is a critical factor in the persistence of H. pylori infections and is a primary contributor to the failure of standard triple or quadruple antibiotic therapies (Grande et al., 2015). Therapeutic strategies targeting the ECM aim to disrupt its structural integrity or prevent its formation, thereby sensitizing the bacteria to conventional antibiotics. Agents such as N-acetylcysteine are used to break down the matrix, while experimental treatments focus on enzymatic degradation of eDNA or inhibition of the signaling pathways that trigger biofilm production (Cammarota et al., 2012). Effectively targeting the H. pylori biofilm is essential for eradicating chronic infections and reducing the risk of associated conditions like peptic ulcers and gastric adenocarcinoma.
Disruption of the extracellular polymeric substance (EPS) matrix, degradation of extracellular DNA (eDNA), and inhibition of quorum sensing to enhance antibiotic penetration and bacterial clearance (Hathroubi et al., 2018; Cammarota et al., 2012).
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