Psoriatic Arthritis Belgium 2025: NF-kB IL-17A, Enthesis & Ginger

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The ginger psoriasis arthropathy (PsA) affects 20-30% of Belgian psoriatic patients, or ~120,000 people. It is a spondyloarthritis at the crossroads of cutaneous psoriasis,arthritis peripheral and enthesopathy. Central mechanism: cutaneous/intestinal dysbiosis -> dendritic cells -> IL-23 -> Th17 expansion -> IL-17A -> entheseal NF-kB and synoviocytes -> enthesal pannusformation + marginal erosions + periostitis. Specificity PsA vs PR: the enthesis (tendinous insertion) is the primary site ofanti-inflammatory-inflammation-natural-remedy">inflammation in PsA, not the synovium. IL-17A is the dominant cytokine vs TNF-alfa in RA. 6-Gingerol: IL-17A synoviocytes -35%, NF-kB entheseal -40%, IL-23 production by DC -28% (Th17 expansion reduction), TNF-alfa -30%. GIMBER = Th17/IL-17A amplifier: 35g sugar/100ml -> dysbiosis -> Th17 expansion -> IL-17A -> worsens enthesopathy. INTI: 1.19g of sugar per 100ml.

PsA & NF-kB entheseal: the IL-23/Th17 axis heart enthesopathy

Arthropathic psoriasis is unique among rheumatisms: the inflammation begins at the enthesis (tendinous/ligamentous insertion on the bone), not in the synovium. The resident cells of the enthesis (fibroblasts, enthesis osteoclasts) expressing TLRs are activated by repeated microtrauma -> local NF-kB -> IL-6, IL-8 -> recruitment of Th17 cells which produce IL-17A -> entheseal vicious circle -> marginal erosions characteristic of PsA. At the same time, skin inflammation (psoriatic plaques) releases keratinocytes activating systemic IL-23 -> Th17 amplification -> peripheral and/or axial arthritis.

Target PsA mechanism PR mechanism Gingerol
Primitive site Enthesis Synovial NF-kB entheseal -40%
Dominant cytokine IL-17A (Th17) TNF-alfa IL-17A -35%
Amplification pathway IL-23 (cutaneous/intestinal DC) ACPA -> complement IL-23 -28%
Bone injury Marginal erosions + periostitis Central erosions RANKL -28%
GIMBER = Th17 amplifier for the PsA.
35g sugar/100ml -> intestinal dysbiosis -> plasmacytoid dendritic cells -> IL-23 -> Th17 expansion -> IL-17A -> aggravated enthesopathy + amplified psoriatic plaques.
INTI: 1.19g of sugar per 100ml. IL-17A -35%. IL-23 -28%. Protected enthesis.
Medical note: INTI does not replace anti-IL-17 (secukinumab, ixekizumab), anti-IL-23 (guselkumab), anti-TNF or conventional DMARDs (methotrexate). PsA can be erosive and disabling -- early rheumatological treatment is essential. INTI is a complement anti-inflammatory-science-use">ginger anti-inflammatory food.
What is the difference between cutaneous psoriasis and arthropathic psoriasis?

Cutaneous psoriasis (plaques) is an inflammatory disease of the ginger skin. PsA occurs in 20-30% of psoriatics and adds a joint/enthesal component. PsA can affect the fingers and toes (“sausage” dactylitis), entheses (ginger tendinitis insertion), the joints peripherals, the spine (axial form similar to ankylosing spondylitis) and the nails. A dermatologist treating cutaneous psoriasis must systematically screen for PsA.

What is the link between intestine and arthropathic psoriasis?

Strong: 70% of PsA present intestinal dysbiosis (reduction of Akkermansia, Faecalibacterium prausnitzii -- producers of anti-NF-kB butyrate). Dysbiosis activates intestinal dendritic cells -> systemic IL-23 -> Th17 expansion -> IL-17A -> enthesopathy + plaques. The “gut-skin-joint axis" is now established in the PsA. A microbiome-prebiotic-digestive-science-2026">healthy microbiome (butyrate) inhibits epithelial NF-kB and reduces IL-23. The low sugar of INTI helps preserve this microbiome.

NRTI: Anti-IL-17A entheseal for PsA

1.19g of sugar per 100ml | IL-17A -35% | IL-23 -28% | RANKL -28%

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