Advanced psoriasis in Belgium: sugar, IL-17, Th17 and ginger (2025)

Epidemiology: Psoriasis in Belgium

• 2–3% of the Belgian population or ~250,000 patients (Psoriasis Belgium Association)
• Plaque psoriasis: 80–90% of cases
• Psoriatic arthritis: 20–30% of psoriasis patients develop joint involvement
• Significantly increased cardiovascular, metabolic, and psychiatric comorbidities
• INAMI reimbursement for biologics (adalimumab, secukinumab, ixekizumab, guselkumab) for PASI ≥10

The Immunopathological Cascade of Psoriasis

1. IL-23/Th17/IL-17 Axis: The Pillar of Psoriasis

Psoriasis is a Th17-dominant disease:

• Plasmacytoid dendritic cells (pDC) → IFN-α → myeloid DC activation
• Myeloid DC → IL-23 → naive CD4+ differentiation → Th17
• IL-17A (Th17) → keratinocytes → NF-κB → β-defensins, CCL20, CXCL1, IL-8
• β-defensins → mast cells/basophils → inflammatory amplification
• IL-17A → keratinocytes → hyperproliferation (keratinocyte turnover 4 days instead of 28 days)
• IL-17A → dermal angiogenesis (VEGF ↑) → psoriatic erythema
• Sugar → dysbiosis → LPS → TLR4 DC → IL-23 ↑ → Th17 ↑ → IL-17A ↑

2. Keratinocyte NF-κB and Hyperproliferation

• IL-17A + TNF-α (synergy) → IKK → IκB degradation → NF-κB p65/p50
• NF-κB → KGF (keratinocyte growth factor), IL-6, IL-8, ICAM-1
• NF-κB → anti-apoptotic (Bcl-2 ↑, survivin ↑) → accelerated proliferation + apoptosis resistance
• AGE (glycation by sugar) → RAGE → keratinocyte NF-κB → direct amplification

3. TNF-α and Dendritic Cells

• TNF-α (Th1 + dermal macrophages) → NF-κB → DC activation → new IL-23 cycle
• TNF-α inhibits FoxP3/Treg → less immune regulation → self-amplification
• Sugar → systemic NF-κB → TNF-α ↑ → psoriatic aggravation

4. Gut-Skin Axis: The Microbiome Hypothesis

• Psoriatic patients: specific dysbiosis (Faecalibacterium prausnitzii ↓, candida-<a%20href=" https:>candida-antifongique-mycose">ginger Candida ↑)
• Sugar → Candida albicans proliferation (sugar is Candida's substrate) → β-glucan → TLR2 → IL-23 ↑
• Zonulin ↑ (intestinal permeability) in psoriatics → systemic LPS → cutaneous NF-κB
• Ginger → mild anti-fungal Candida (6-gingerol) → dysbiosis ↓ → IL-23 ↓
• Ginger → zonulin ↓ → tight junctions → LPS ↓ → cutaneous NF-κB ↓

Ginger and Psoriasis: Scientific Basis

• 6-gingerol → keratinocyte NF-κB ↓ → ↓ IL-8, ↓ CXCL1 → less cutaneous neutrophils
• 6-shogaol → TNF-α ↓ → less TNF-α/IL-17 synergism → hyperproliferation ↓
• 2022 study: topical ginger application → ↓ PASI (Psoriasis Area Severity Index) in murine model
• Curcumin (INTI) + gingerol: NF-κB ↓ synergy, Th17 ↓ → complementarity in psoriasis

⚠️ Psoriasis Medication Interactions

• Anti-TNF (adalimumab, etanercept): ginger is a mild antiplatelet → inform dermatologist
• Systemic methotrexate: possible hepatic interaction → discuss with dermatologist
• Biologics IL-17i/IL-23i: no documented interaction — INTI generally compatible