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Pathogen adhesion to the mucosal surface is the fundamental initial step in the pathogenesis of most infectious diseases, serving as the gateway for colonization and subsequent tissue invasion (Nature Reviews Microbiology, 2017). This process is mediated by the specific interaction between microbial surface structures, known as adhesins (such as pili, fimbriae, or viral glycoproteins), and complementary host receptors, which are typically glycans or proteins on the apical surface of epithelial cells (Frontiers in Cellular and Infection Microbiology, 2011). By anchoring to the mucosa, pathogens can resist the mechanical flushing actions of fluids like mucus, urine, or saliva, allowing them to establish a niche and potentially form biofilms (NIH, 2021). Therapeutic intervention targeting this process, known as anti-adhesion therapy, utilizes small molecules, carbohydrate mimetics, or monoclonal antibodies to block these interactions (PubMed, 2016). This approach is particularly valuable as it often targets the pathogen's ability to cause disease rather than its viability, potentially reducing the selective pressure for the development of antimicrobial resistance (Journal of Clinical Investigation, 2013). Common examples of drugs targeting this mechanism include FimH inhibitors for urinary tract infections and viral entry inhibitors for HIV or RSV (ClinicalTrials.gov, 2023). Overall, understanding the molecular basis of adhesion is crucial for developing next-generation anti-infectives that preserve the host's commensal microbiome.
Inhibition of microbial attachment to host mucosal receptors through competitive binding or steric hindrance (Nature Reviews Microbiology, 2017).
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