Microbial–Host Interactions in Dermatologic Inflammation: Ecological, Immunological, and Clinical Perspectives
DOI:
https://doi.org/10.64784/050Keywords:
Skin microbiome, inflammatory dermatoses, Dysbiosis, innate immunity, Th2/Th17 pathways, microbial–host interactionsAbstract
Inflammatory skin diseases are increasingly understood through the lens of the cutaneous microbiome, a dynamic ecosystem whose interactions with the host shape immune responses, barrier integrity, and clinical disease expression. This review synthesizes evidence from two decades of research to examine how microbial composition, functional dysbiosis, and host–microbe crosstalk contribute to the pathophysiology of atopic dermatitis, psoriasis, acne, rosacea, and Malassezia-associated dermatoses. The findings demonstrate that innate immune mechanisms—particularly barrier components, antimicrobial peptides, and pattern recognition receptors—form the primary interface between the microbiome and the host, while disease-specific adaptive pathways (Th2 in atopic dermatitis, Th17 in psoriasis) define distinct inflammatory phenotypes. Temporal trends reveal a rapid expansion of microbiome research beginning in the late 2010s, driven by advances in sequencing and molecular immunology, while thematic analysis highlights an imbalance between mechanistic studies and the still limited development of microbiome-based therapies. The review also identifies a critical gap concerning the underrepresentation of diverse populations, especially in regions such as Mexico, Colombia, and Ecuador, where environmental and cultural factors significantly influence microbial ecology. Collectively, the evidence underscores the microbiome’s central role in shaping cutaneous inflammation and emphasizes the need for geographically inclusive research and translational innovation to support future dermatologic practice.
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