Staphylococcus aureus adhesion to human epidermis

Staphylococcus aureus adhesion to the human epidermis is a complex biological process rather than a single molecular target, serving as the critical initial step for bacterial colonization and subsequent infection [1]. This process is primarily mediated by a family of bacterial surface proteins known as Microbial Surface Components Recognizing Adhesive Matrix Molecules (MSCRAMMs), most notably Iron-regulated surface determinant protein A (IsdA) and Clumping factor B (ClfB) [1, 2]. These bacterial proteins specifically bind to host ligands within the stratum corneum, such as loricrin, involucrin, and cytokeratin 10, which are often more accessible in patients with skin barrier defects [2, 3]. In clinical contexts like atopic dermatitis, the high density of S. aureus colonization driven by these adhesive interactions correlates with disease severity and inflammatory flares [3, 4]. Therapeutic interventions targeting this process, such as monoclonal antibodies or small-molecule inhibitors, aim to prevent the pathogen's attachment to host tissues, thereby reducing the risk of invasive infection and minimizing the disruption of the normal skin microbiome [1, 4]. While traditional antibiotics like mupirocin are used for decolonization, novel anti-adhesion strategies are being explored to provide more targeted therapy with a lower risk of promoting antimicrobial resistance [1, 3]. Sources: [1] Clarke, S. R., et al. (2007). Iron-regulated surface determinant protein A (IsdA) is needed for Staphylococcus aureus adhesion to human skin. Journal of Biological Chemistry. [2] O'Brien, L. M., et al. (2002). Staphylococcus aureus clumping factor B (ClfB) promotes adherence to human loricrin. Molecular Microbiology. [3] Geoghegan, J. A., et al. (2018). Staphylococcus aureus and atopic dermatitis: a complex and evolving relationship. British Journal of Dermatology. [4] Weidenmaier, C., et al. (2004). Role of teichoic acids in Staphylococcus aureus nasal colonization. Nature Medicine.

Other names

S. aureus skin colonizationStaphylococcal epidermal attachmentS. aureus-host cell adhesion

Inhibition of bacterial surface proteins (MSCRAMMs) from binding to host epidermal ligands such as loricrin, involucrin, and cytokeratin 10.