Bacterial adhesion at the skin surface

Bacterial adhesion at the skin surface is the critical initial step in the colonization and subsequent pathogenesis of cutaneous infections. This complex process is primarily mediated by a family of bacterial surface proteins known as Microbial Surface Components Recognizing Adhesive Matrix Molecules (MSCRAMMs), which include clumping factors (ClfA/B) and fibronectin-binding proteins (FnbpA/B) that anchor pathogens like Staphylococcus aureus to host extracellular matrix components or keratinocyte receptors. In pathological conditions such as atopic dermatitis, the skin barrier is compromised, leading to the exposure of ligands like loricrin and corneodesmosin, which serve as high-affinity docking sites for these bacterial adhesins, facilitating persistent colonization and inflammatory flares. Targeting the molecular mechanisms of adhesion represents a novel therapeutic paradigm, often termed anti-adhesion therapy, which aims to prevent infection without the strong selective pressure for resistance associated with traditional bactericidal antibiotics. Current and emerging interventions include monoclonal antibodies like tefibazumab, competitive inhibitors such as specific sugars, and topical formulations designed to disrupt the 'catch bonds' that strengthen bacterial attachment under mechanical stress.

Other names

Microbial skin attachmentBacterial colonization of the skinBiofilm initiation on skinCutaneous bacterial adherenceMicrobial adhesion to the epidermis

Inhibition of bacterial attachment to host ligands (such as fibronectin, collagen, or loricrin) through competitive binding by carbohydrate or peptide analogs, antibody-mediated neutralization of bacterial adhesins, or modification of the skin's physicochemical properties to prevent microbial docking.