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Gardnerella vaginalis adhesion to vaginal epithelial cells is a key pathogenic step in the development of bacterial vaginosis, facilitating biofilm formation, persistence, and resistance to host defenses and antibiotics[6][5][1]. Adhesion is mediated by bacterial virulence factors, such as sialidase (which degrades the protective mucus layer to enable binding) and vaginolysin (a pore-forming cytotoxin that interacts with host cell membranes and complement factors)[6][4]. The process is essential for colonization and biofilm formation, which are associated with epithelial cell apoptosis, disruption of mucosal barrier integrity, and subsequent clinical complications such as increased risk of infection, inflammation, and adverse pregnancy outcomes[5][3]. Therapies (such as metronidazole and clindamycin) target bacterial growth, but biofilm-associated infections remain a significant therapeutic challenge with frequent relapses[6][1].
Inhibition of bacterial growth and biofilm formation (metronidazole, clindamycin); Possible reduction of adhesive capacity at subinhibitory concentrations (metronidazole)
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