Cutibacterium acnes adhesion to skin cells

Cutibacterium acnes adhesion to skin cells is a fundamental biological process and a key therapeutic target in the management of acne vulgaris. This interaction is primarily mediated by bacterial surface proteins known as adhesins, including Dermatan-sulfate adhesins (DsA1 and DsA2), which facilitate binding to host keratinocytes and sebocytes (PubMed: 25667173). Successful adhesion allows C. acnes to colonize the pilosebaceous unit and initiate the formation of biofilms, which provide a protective environment against host immune defenses and antimicrobial agents (PubMed: 29330344). Furthermore, the attachment of C. acnes triggers pro-inflammatory signaling pathways through the activation of Toll-like receptors (TLR2 and TLR4), leading to the release of cytokines such as IL-8 and the subsequent development of inflammatory acne lesions (PubMed: 30634430). Therapeutic strategies targeting this process aim to inhibit bacterial attachment using small molecules, peptides, or natural compounds like Epigallocatechin-3-gallate, thereby preventing colonization without necessarily exerting broad-spectrum bactericidal effects (PubMed: 23038065). This approach is considered a promising 'microbiome-friendly' alternative to traditional antibiotics, as it may reduce the selective pressure for resistance while maintaining the skin's ecological balance (PubMed: 31403865).

Other names

Propionibacterium acnes adhesionC. acnes attachmentBacterial adhesion to keratinocytesC. acnes-host cell interactionC. acnes biofilm initiation

Adhesion inhibition, competitive binding to host receptors, and disruption of bacterial surface protein interactions.