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The adhesion of *Cutibacterium acnes* (formerly *Propionibacterium acnes*) to human tissues is mediated by specific cell-surface proteins known as adhesins, notably DsA1, which recognize and bind to host molecules including dermatan sulfate and fibrinogen[3][5]. This process is critical for bacterial colonization, biofilm formation, and the pathogenesis of conditions such as acne vulgaris and device-associated infections[4][5]. The molecular characterization of DsA1 reveals a large glycosylated protein with diverse domains facilitating host interaction, including a signal peptide, LPXTG cell-wall anchoring motif, and repeat regions[3]. Inhibition of these adhesins is a potential avenue for preventing or treating infection and inflammation driven by *C. acnes*[5][3].
Inhibition of bacterial binding to host tissue proteins (e.g., dermatan sulfate, fibrinogen). Blocking biofilm formation.
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