Staphylococcus epidermidis surface proteins (MSCRAMMs)

Staphylococcus epidermidis surface proteins, often referred to as surface receptors or adhesins, are a diverse group of cell wall-anchored (CWA) molecules that mediate the bacteria's interaction with its environment [2, 12]. The most prominent members belong to the Microbial Surface Components Recognizing Adhesive Matrix Molecules (MSCRAMMs) family, including SdrG (fibrinogen-binding), SdrF (collagen-binding), and SdrH, which facilitate the initial adherence of the bacteria to host extracellular matrix components and the surfaces of indwelling medical devices [7, 16, 18]. Other key proteins include the accumulation-associated protein (Aap) and the extracellular matrix binding protein (Embp), which are essential for the accumulation phase of biofilm formation and contribute to immune evasion by protecting the bacteria from host defenses [5, 10, 11]. These surface structures are primary therapeutic targets because they are critical for the colonization and persistence of S. epidermidis in the host [12, 17]. In clinical settings, S. epidermidis is a leading cause of opportunistic nosocomial infections, particularly catheter-related bloodstream infections, prosthetic joint infections, and neonatal sepsis [12, 14, 15]. Therapeutic interventions targeting these receptors include monoclonal antibodies like Pagibaximab (which targets the associated lipoteichoic acid) and experimental vaccines designed to block adhesion or promote opsonophagocytic killing [3, 6, 8, 16]. However, the development of effective therapies is complicated by the significant genetic diversity among S. epidermidis strains and the functional redundancy among different surface proteins, which can allow the pathogen to bypass single-target inhibitors [2, 15, 17].

Other names

Staphylococcus epidermidis surface receptorsS. epidermidis adhesinsCell wall-anchored proteinsCWA proteinsMicrobial Surface Components Recognizing Adhesive Matrix Molecules

Inhibition of bacterial adhesion to host tissues and medical devices, promotion of opsonophagocytic killing by host immune cells, and disruption of biofilm formation and maintenance [3, 8, 16].