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Bacteria adhesion to host cells refers to the initial and often critical attachment step by which bacteria bind to surface molecules (receptors) on host cells, initiating colonization and infection. This process generally involves bacterial surface proteins called adhesins—often located on fimbriae, pili, or are afimbrial in nature—that specifically recognize and bind diverse host cell receptors, sometimes via bridging molecules such as fibronectin or integrins[1][2][3][4][5]. Adhesion can occur through complex, multi-step processes involving direct and indirect interactions and is tightly regulated by both microbial and host cell features, including the glycocalyx barrier and cytoskeletal dynamics[1][2][4][5]. Because this process is central to pathogenesis, the adhesin-receptor interface is an attractive but mechanistically diverse target for anti-infective strategy development. Key clarification: To index a therapeutically actionable "target," one must refer to a specific adhesin (e.g., FimH, Invasin, fibronectin-binding protein [FnBP]) or a specific host receptor (e.g., β1-integrin, fibronectin, CD80, etc.), not the generalized process of adhesion itself[1][2][3][4][5].
Mechanisms described for adhesion inhibitors include blocking adhesin-receptor interaction, inhibiting pilus assembly or function, or masking host cell receptors[1][2][3][4].
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