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Free calcium ions (Ca2+) are essential structural and signaling components within the bacterial biofilm matrix (Patrauchan et al., 2005, Journal of Bacteriology). They function primarily by cross-linking negatively charged extracellular polymeric substances (EPS), such as alginate and extracellular DNA (eDNA), which provides the biofilm with mechanical stability and resistance against host immune responses and antibiotics (Whitchurch et al., 2002, Science). High concentrations of calcium are frequently observed in chronic infection sites, such as the lungs of cystic fibrosis patients, where they promote the transition of bacteria like Pseudomonas aeruginosa into a sessile, biofilm-protected state (Glick et al., 2010, Journal of Bacteriology). Calcium also acts as a secondary messenger in bacterial signaling pathways that regulate virulence factor production and biofilm maturation (Domenech et al., 2015, Frontiers in Microbiology). Therapeutic strategies targeting these ions involve the use of chelating agents like EDTA or citrate to sequester Ca2+, thereby weakening the matrix architecture (Banin et al., 2006, Applied and Environmental Microbiology). This destabilization facilitates the penetration of conventional antibiotics and promotes the clearance of the infection (Percival et al., 2005, Journal of Wound Care).
Chelation and sequestration of divalent cations to disrupt the structural integrity of the extracellular polymeric substance (EPS) matrix (Banin et al., 2006, Applied and Environmental Microbiology).
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