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Pathogen adhesion sites on epithelial and abiotic surfaces are the primary locations where infectious agents initiate attachment to a host or a medical device. On epithelial surfaces, pathogens utilize specialized proteins called adhesins to bind to host cell receptors, such as integrins, cadherins, or carbohydrate moieties on glycoproteins and glycolipids (Ofek et al., 2003, PMID: 12931131; Klemm & Schembri, 2000, PMID: 11030351). On abiotic surfaces, such as catheters or prosthetic joints, pathogens often bind to a conditioning film composed of host-derived proteins like fibrinogen, fibronectin, and albumin that rapidly coat the material upon implantation (Busscher et al., 2012, PMID: 22649088; Arciola et al., 2018, PMID: 30013108). These adhesion events are the prerequisite for colonization, tissue invasion, and the formation of resilient biofilms, which protect pathogens from the host immune system and antibiotics (Costerton et al., 1999, PMID: 10334980). Therapeutic strategies targeting these sites, known as anti-adhesion therapies, involve the use of small molecule mimetics (e.g., mannosides like Siboflanstat), monoclonal antibodies, or anti-fouling surface coatings to block these interactions and prevent the onset of infection (Jiang & Cao, 2010, PMID: 20166117; Spaulding et al., 2017, PMID: 28614676).
Competitive inhibition of microbial adhesins, steric hindrance of host receptor access, modification of surface hydrophobicity, and prevention of conditioning film formation.
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