The Role of Skin Microbiota in Facial Dermatoses and Related Factors: A Narrative Review

Inflammatory facial dermatoses (atopic dermatitis [AD], acne vulgaris, contact dermatitis, seborrheic dermatitis, rosacea, perioral dermatitis, and demodicosis, etc.) often profoundly impact patients' appearance and psychological well-being. In this narrative review, we wanted to present the current knowledge on the role of skin microbiota in common facial dermatoses. Skin keratinocytes are the primary producers of antimicrobial peptides (AMPs) and express Toll-like receptors (TLRs), which stimulate the T helper (Th1) immune response, with the production of interferon (IFN). They can also produce certain pro-inflammatory cytokines, namely IL-1β, IL-18, IL-6, IL-10, and the tumor necrosis factor (TNF). In healthy infants, the bacterial skin microbiota is predominantly composed of Firmicutes (genera Staphylococcus and Streptococcus), as well as Actinobacteria, Proteobactera, and Bacteroidota. The genera Cutibacterium and Staphylococcus, which have antimicrobial effects and compete with pathogens for nutrients/ecological niches, coexist symbiotically on the skin and can reduce the expression of TLR2 and TLR4. In patients with AD, lesional/non-lesional skin was found to have increased colonization by Staphylococcus aureus which reduces effector T lymphocytes' ability to produce cytokines, such as IL-17A and IFN-γ, leading to decreased AMP production and impaired skin microbiota immune functionality. In patients with rosacea, the overexpression of TLR2 may stimulate elevated pro-inflammatory cytokine production (IL-8, IL-1β, and TNF-α, etc.), exacerbating the inflammatory response. Also, increased colonization by Malassezia yeasts triggers a Th2 immune response and cytokine secretion (IL-1α, IL-1β, IL-2, IL-4, IL-6, IL-8, IL-10, IL-12, TNF-α, beta-defensin, IFN-γ, nitric oxide, and histamine), and participates in signaling pathways. Insight into these factors may further improve clinical approaches to patients with facial dermatoses.