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Bacterial surface receptors on DFU-associated pathogens represent a broad class of molecules, including adhesins and Microbial Surface Components Recognizing Adhesive Matrix Molecules (MSCRAMMs), that facilitate the colonization of diabetic foot ulcers. These receptors are expressed by common DFU pathogens such as Staphylococcus aureus, Pseudomonas aeruginosa, and Enterococcus faecalis, enabling them to bind to host extracellular matrix proteins like collagen, fibrinogen, and fibronectin. This binding is a critical first step in the establishment of chronic infections and the formation of resilient biofilms, which protect bacteria from the host immune system and systemic antibiotics. In the context of diabetic foot ulcers, these receptors are therapeutic targets for both traditional antibiotics and novel anti-adhesion strategies. By blocking these surface interactions, it is possible to prevent bacterial attachment and disrupt the maturation of biofilms, thereby improving wound healing outcomes and reducing the risk of lower-limb amputation. However, the high diversity of bacterial species and the rapid evolution of surface proteins present significant challenges for targeted molecular therapies.
Antibiotics typically inhibit cell wall synthesis, protein synthesis, or DNA replication after binding to or bypassing surface structures; anti-adhesion therapies competitively inhibit these receptors to prevent colonization and biofilm formation.
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