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The mammalian skin cell components and commensal skin microbiota constitute a multi-layered biological system essential for maintaining cutaneous homeostasis and barrier function. The host component includes specialized cells such as keratinocytes, which form the physical stratum corneum, and resident immune cells like Langerhans cells that mediate inflammatory responses (Byrd et al., 2018, Nature Reviews Microbiology). This environment is colonized by a vast array of commensal bacteria, fungi, and viruses, collectively known as the skin microbiota, which compete with pathogens and produce antimicrobial peptides (Grice & Segre, 2011, Nature Reviews Microbiology). Interactions between these microbes and host cells are critical for immune maturation and wound healing. Disruptions to this ecosystem, known as dysbiosis, are central to the pathogenesis of diseases like atopic dermatitis, where Staphylococcus aureus overgrowth exacerbates inflammation (Chen et al., 2018, Nature Reviews Microbiology). Pharmacological interventions targeting this system range from traditional antimicrobials and corticosteroids to modern microbiome-modulating therapies and biologics that restore the skin's protective landscape.
Modulation of microbial populations and host immune-epithelial signaling to restore skin barrier integrity and reduce inflammation.
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