Ha Eun Kim
Jeonbuk National University Medical School, Republic of Korea
Abstract Title:
The repurposing of nitazoxanide for psoriasis treatment exerts therapeutic effects through skin metabolic reprogramming
Biography:
Ha Eun Kim is a PhD student in the Department of Immunology at Jeonbuk National University Medical School, Republic of Korea. Her research focuses on immunometabolism and immune regulation in inflammatory diseases, including psoriasis, atopic dermatitis, osteoarthritis, and regulatory B cell-mediated immune responses. She investigates metabolic signaling pathways and drug repurposing strategies to identify novel therapeutic targets for immune-mediated diseases. She has published multiple SCI papers in international journals and continues to explore the role of immunometabolism in the pathogenesis and treatment of inflammatory disorders.
Research Interests:
Psoriasis is a chronic inflammatory skin disease characterized by excessive keratinocyte proliferation, immune dysregulation, and metabolic alterations. Recent studies have highlighted immunometabolic reprogramming as a critical mechanism underlying disease progression, suggesting that metabolic pathways represent promising therapeutic targets. Nitazoxanide (NTZ), an FDA-approved antiparasitic drug, has recently emerged as a potential immunometabolic regulator. In this study, we investigated the therapeutic effects and underlying mechanisms of NTZ using IL-17A-stimulated primary human keratinocytes and imiquimod-induced psoriasis-like mouse models. NTZ significantly reduced the expression of psoriasis-associated inflammatory mediators and antimicrobial peptides while suppressing glucose metabolism and restoring mitochondrial function. Mechanistically, NTZ activated AMPK signaling and inhibited mTORC1 activity, leading to metabolic normalization and attenuation of inflammatory responses. In vivo administration of NTZ markedly improved psoriasis-like skin inflammation, reduced epidermal hyperplasia, and decreased inflammatory cell infiltration. Furthermore, NTZ suppressed pathogenic Th17 responses and promoted immune homeostasis in psoriatic skin lesions. These findings demonstrate that NTZ alleviates psoriasis through regulation of skin metabolic reprogramming via the AMPK/mTORC1 pathway and provide evidence supporting drug repurposing of NTZ as a novel therapeutic strategy for psoriasis and other inflammatory skin diseases.
