Skin microbiome–inflammatory pathways axis

The concept of “skin microbiome & inflammatory pathways” does not refer to a single molecule or canonical therapeutic target, but rather describes the complex interplay between the diverse community of microorganisms (bacteria, fungi, viruses) on the skin and the host’s immune and inflammatory signaling pathways[1][2][3][4][5]. The skin microbiome maintains homeostasis and provides protection against pathogens by modulating innate and adaptive immune responses, including the secretion of antimicrobial peptides, cytokines, and chemokines via direct microbe–host interactions[2][3][4]. Dysbiosis—an imbalance of the microbial community—can contribute to the initiation and maintenance of inflammatory skin diseases such as atopic dermatitis, seborrheic dermatitis, psoriasis, rosacea, and acne, partly by altering barrier function, stimulating inappropriate immune responses, and increasing the production of pro-inflammatory cytokines by both microbes (e.g., toxins from Staphylococcus aureus) and host cells (e.g., keratinocytes, dendritic cells)[1][3][4][5]. Recent therapeutic strategies involve targeted modulation of the skin microbiome (e.g., bacteriotherapy using beneficial commensals or engineered strains) to restore balance, limit inflammation, and support the skin’s defensive capacity[4]. This entry is considered incorrect as a therapeutic “target” since it does not correspond to a specific molecule, protein, receptor, enzyme, or defined molecular entity, but rather an ecosystem process and functional axis. It should be replaced by more precise molecular targets within the described pathways, such as “Toll-like receptor 2,” “Staphylococcus aureus alpha-toxin,” or “Interleukin-17.”

Other names

skin microbiome and inflammationskin microbiota–immune axis

Modulation of microbial composition to restore balance (dysbiosis correction); Reduction of pathogenic bacteria to limit their toxin production and inflammatory effects; Stimulation or restoration of commensal bacteria that promote anti-inflammatory signals and antimicrobial peptide (AMP) production; Enhancement of endogenous glucocorticoid synthesis via host-microbe signaling