Skin microbiome dysbiosis

Skin microbiome dysbiosis refers to an **imbalance** in the composition and function of microorganisms residing on the skin surface. This condition is characterized by reduced diversity or overgrowth/dominance by specific pathogenic species—such as *Staphylococcus aureus* in atopic dermatitis or *Cutibacterium acnes* in acne—which can disrupt normal immune responses and barrier functions. Dysbiosis has been linked to numerous dermatological diseases including eczema/atopic dermatitis, psoriasis, acne vulgaris, rosacea, seborrheic dermatitis/dandruff, impaired wound healing, vitiligo and other autoimmune conditions affecting the skin. The precise cause-effect relationship remains under investigation—dysbiosis may be both a driver and consequence of disease processes. Therapeutic strategies focus on restoring healthy microbial balance using topical/oral probiotics that introduce beneficial bacteria; prebiotic compounds that nourish commensals; postbiotic products containing non-living bacterial components/metabolites with immunomodulatory effects; phage therapy targeting specific pathogens without harming commensals; experimental approaches like skin microbiota transplants are also being explored. Diagnosis typically involves sequencing-based assessment rather than single-molecule biomarkers. Importantly—**skin microbiome dysbiosis is not itself a discrete molecular target**, receptor or protein but describes an altered ecological state within the cutaneous microbial community. Thus it does not fit standard definitions used for drug targets such as receptors or enzymes.

Other names

Dysbiosis of the skin microbiomeCutaneous microbiome imbalanceSkin microbial dysbiosis

Mechanisms relate to restoration of microbial balance rather than direct molecular targeting. - Competitive exclusion of pathogens by beneficial microbes - Modulation of immune responses via microbial metabolites/postbiotics - Enhancement of skin barrier function through microbe-derived factors