Psoriasis is a chronic inflammatory skin disease characterized by keratinocyte hyperactivation and dysregulated cytokine signaling, with nuclear factor kappa B (NF-κB), a master transcription factor that regulates immune and inflammatory gene expression, playing a central role. Adalimumab, a monoclonal antibody that inhibits tumor necrosis factor alpha (TNF-α), is widely used in psoriasis therapy, yet its molecular effects on NF-κB-associated genes and microRNAs (miRNAs) in keratinocytes remain insufficiently defined. In this study, immortalized human keratinocytes (HaCaT cells) were exposed to lipopolysaccharide (LPS) to induce inflammatory stress and treated with adalimumab for 2, 8, and 24 h. Transcriptome-wide profiling was performed using messenger RNA (mRNA) and miRNA microarrays, followed by validation with reverse transcription quantitative polymerase chain reaction (RT-qPCR) and enzyme-linked immunosorbent assay (ELISA). Bioinformatic analyses included prediction of miRNA–mRNA interactions, construction of protein–protein interaction (PPI) networks, and gene ontology (GO) enrichment. Adalimumab reversed LPS-induced upregulation of NF-κB-associated genes, including inhibitor of nuclear factor kappa-B kinase subunit beta (IKBKB), interleukin-1 receptor-associated kinase 1 (IRAK1), TNF receptor-associated factor 2 (TRAF2), mitogen-activated protein kinase kinase kinase 7 (MAP3K7), and TNF alpha-induced protein 3 (TNFAIP3), with concordant changes observed at the protein level. Several regulatory miRNAs, notably miR-1297, miR-30a, miR-95-5p, miR-125b, and miR-4329, showed reciprocal expression changes consistent with anti-inflammatory activity. STRING analysis identified IKBKB as a central hub in the PPI network, while GO enrichment highlighted immune regulation, apoptosis, and NF-κB signaling. These findings demonstrate that adalimumab modulates NF-κB activity in keratinocytes through coordinated regulation of gene, protein, and miRNA expression, providing mechanistic insight into TNF-α blockade in psoriasis.

Background/Objectives: Psoriasis is a chronic immune-mediated disease frequently accompanied by systemic inflammation and metabolic disturbances. Nutrition plays a crucial role in modulating inflammatory pathways, yet the impact of baseline dietary status on systemic therapy outcomes remains underexplored. Methods: A total of 37 patients (20 men, 17 women; mean age 47.8 ± 4.87 years) scheduled for cyclosporine A (CsA) therapy underwent dietary assessment using 24 h recall and food frequency questionnaires. Intake was compared with dietary reference values. Psoriasis severity was measured by using the Psoriasis Area and Severity Index (PASI) and Body Surface Area (BSA) at baseline, day 42, and day 84. Mixed-effects regression models adjusted for body mass index (BMI), age, and sex assessed associations between nutrient adequacy and clinical outcomes. Results: Participants exhibited frequent dietary imbalances, including low polyunsaturated fatty acids, fiber, vitamin D, folate, and minerals such as magnesium and zinc, alongside excess saturated fat and sodium. Adequate intake of fiber, eicosapentaenoic acid (EPA)+ docosahexaenoic acid (DHA), and vitamins A and D, folate, magnesium, and zinc was independently associated with a lower baseline PASI/BSA and faster improvement during CsA therapy (p < 0.05). Higher BMI, older age, and male sex predicted poorer outcomes. Conclusions: Pre-treatment nutritional inadequacies are common in psoriasis and independently predict diminished therapeutic response to CsA. Early nutritional optimization may enhance treatment efficacy and support long-term disease control. Integrating dietary assessment in psoriasis management represents a feasible, impactful adjunct to pharmacotherapy.

Background: Psoriasis vulgaris is a systemic immune-mediated disease marked by oxidative stress and disruptions in mineral homeostasis. This study evaluated the effect of 12-week cyclosporine A (CsA) therapy on serum micro-/macroelements and redox balance in adults with moderate–severe disease. Methods: Thirty-seven patients were prospectively assessed at baseline, day 42, and day 84. Disease severity was quantified using PASI and BSA. Serum copper, zinc, magnesium, calcium, iron, sodium, and potassium were measured by atomic absorption spectrometry. Total antioxidant status (TAS), total oxidant status (TOS), and oxidative stress index (OSI = TOS/TAS × 100) were determined spectrophotometrically. Results: CsA treatment produced significant clinical improvement, demonstrated by reductions in PASI and BSA. Parallel biochemical changes included decreased copper and increased zinc, magnesium, calcium, and iron levels toward reference ranges (all p < 0.0001). TAS increased, TOS decreased, and OSI was markedly reduced, indicating restored redox balance. The Cu/Zn ratio declined throughout therapy, and elevated magnesium at week 12 correlated with greater clinical improvement. Sodium and potassium levels remained stable. Subgroup analyses suggested differing biochemical responses in smokers, patients with diabetes, and individuals with obesity. Conclusions: CsA improves psoriasis severity while ameliorating systemic oxidative stress and mineral disturbances. The Cu/Zn ratio and serum magnesium may support personalized monitoring during CsA therapy.