Truncal acne significantly impairs quality of life yet remains underexplored relative to facial acne, particularly with respect to fungal ecology. The trunk represents a distinct cutaneous niche characterized by thicker epidermis, larger follicular units, and frequent occlusion, and harbors a high abundance of Malassezia species. In this study, we used internal transcribed spacer 2 (ITS2) amplicon sequencing to characterize the truncal mycobiome in patients with acne and in healthy controls and to compare fungal community features across doxycycline exposure groups. Although serial sampling was planned, seven participants contributed a single follow-up sample after doxycycline treatment, and only two participants contributed multiple follow-up samples sufficient for true within-subject longitudinal analyses; therefore, most analyses represent exposure-stratified cross-sectional comparisons rather than confirmed temporal change. At baseline, truncal acne lesions exhibited increased fungal richness and distinct community composition compared with controls. Acne lesions were more frequently enriched for Malassezia globosa, whereas healthy controls were dominated by M. sympodialis. Across doxycycline exposure groups, fungal communities remained Malassezia-dominant with substantial inter-individual variability. Doxycycline exposure was associated with partial and heterogeneous differences in Malassezia species composition without uniform normalization toward control profiles. Because only fungal sequencing was performed, bacterial–fungal interactions were inferred from prior literature and not directly measured. These findings indicate that truncal acne is associated with a distinct fungal community structure and highlight the need for integrated, longitudinal multi-omics studies to clarify treatment-associated microbial dynamics.
Obesity is increasingly recognized as a systemic pro-inflammatory condition that influences not only metabolic and cardiovascular health but also the development and exacerbation of cutaneous inflammatory diseases. This review examines the interplay between obesity, microbial dysbiosis, and two archetypal inflammatory skin disorders—hidradenitis suppurativa (HS) and psoriasis. We highlight how obesity-induced changes in immune signaling, gut permeability, and microbiota composition—both in the gut and the skin—contribute to cutaneous inflammation. Special emphasis is placed on shared pathways such as the Th17/IL-23 and IL-22 signaling axes, adipokine imbalance, and microbial metabolites like short-chain fatty acids and lipopolysaccharides. The review critically evaluates the current literature, distinguishing preclinical insights from clinical evidence, and underscores the potential of microbiota-targeted therapies and metabolic interventions as adjunctive treatment strategies. By integrating metabolic, immunologic, and microbiome data, we synthesize emerging evidence to better understand the gut–skin–obesity interplay and guide future therapeutic innovations.
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