Gut–Skin–Brain Interactions in Chronic Dermatological Disease: Microbiome, Psychological Stress, and Systemic Inflammation

Abstract

Chronic dermatological diseases are increasingly understood as systemic disorders influenced by interactions among cutaneous and intestinal microbiota, immune regulation, psychological stress, and neuroendocrine signaling. This study analyzed the gut–skin–brain axis as an integrative framework for understanding the pathophysiology of psoriasis, atopic dermatitis, acne, and rosacea. An integrative literature review structured according to the Scientific Method was conducted, incorporating evidence concerning intestinal and cutaneous dysbiosis, epithelial barrier alterations, microbial metabolites, systemic inflammation, psychological stress, hypothalamic–pituitary–adrenal axis activation, autonomic signaling, neuroimmune mechanisms, sleep disturbances, and quality of life. The analysis identified systemic inflammation as the most consistently represented connecting domain across the reviewed evidence. Microbiota-related studies frequently incorporated immune and inflammatory pathways, whereas psychological and neuroendocrine research also demonstrated substantial overlap with inflammatory mechanisms and clinical manifestations. Psoriasis showed a strong representation of microbiota and systemic inflammatory pathways; atopic dermatitis demonstrated prominent interactions among barrier dysfunction, microbial alterations, pruritus, immune activation, and stress; acne showed a relatively balanced distribution among microbial, inflammatory, metabolic, and psychological mechanisms; and rosacea demonstrated relevant inflammatory, neurovascular, microbial, and psychological components. Direct integration of microbiome and psychological variables within the same investigations remained comparatively limited, revealing an important methodological gap. Overall, the findings support the gut–skin–brain axis as a multidirectional and disease-dependent framework rather than a fixed linear pathway. Microbial dysbiosis, inflammatory signaling, stress responses, and cutaneous manifestations appear to interact bidirectionally, although current evidence supports biological plausibility and association more strongly than definitive causality. Future longitudinal and interventional studies should simultaneously evaluate microbiome composition, inflammatory biomarkers, psychological variables, neuroendocrine function, sleep, and dermatological severity to clarify causal pathways and potential therapeutic targets.