IMMUNOPATHOLOGICAL MECHANISMS IN CHRONIC SKIN INFECTIONS: BRIDGING DERMATOLOGICAL AND IMMUNOLOGICAL PERSPECTIVES

Abstract

Chronic skin infections represent a persistent global health burden, often arising from a complex interplay between microbial persistence and dysregulated immune responses. This study investigates the immunopathological mechanisms underlying chronic dermatological infections by integrating quantitative immunological assays, microbiological analyses, and histopathological evaluation within a mixed-methods experimental framework. Blood and lesional tissue samples from patients with chronic bacterial, fungal, and viral infections were analyzed to assess cytokine profiles, immune cell distributions, and microbial loads. Elevated levels of pro-inflammatory cytokines, including IL-1β, IL-6, and TNF-α, were consistently observed, correlating with increased lesion severity and microbial density. Flow cytometric analysis revealed an imbalance in CD4⁺/CD8⁺ T-cell ratios and an expansion of regulatory T cells, indicating sustained immune activation and compensatory immunosuppression. Histopathological examination demonstrated epidermal hyperplasia, dermal fibrosis, and lymphocytic infiltration, confirming the chronic inflammatory milieu. Microbial culture and qPCR assays identified Staphylococcus aureus and Candida albicans as predominant pathogens, with biofilm formation contributing to immune evasion and prolonged infection. Regression and mathematical cytokine diffusion modeling established a predictive relationship between immune hyperactivity and infection chronicity, highlighting the cyclical nature of immune-pathogen interactions. The integrated findings underscore that chronic skin infections are driven by reciprocal reinforcement between immune overactivation and microbial adaptation. This research provides a mechanistic bridge between dermatological and immunological perspectives, offering a foundation for precision therapies that target both pathogen persistence and host immune dysregulation.