Severe Atopic Dermatitis Belgium 2025: NF-kB Keratinocytes, Th2 & Ginger

INTI — Organic Ginger, Turmeric & Lemon Shot

INTI — Organic Ginger, Turmeric & Lemon Shot

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The ginger atopic dermatitis (DA) severe affects 200,000 Belgian adults (3-5% of the population) and represents a considerable burden: intense pruritus, chronic insomnia, psychological impact. Central mechanism: FLG mutation (filaggrin) or barrier dysfunction -> TSLP + IL-33 (alarmins) by keratinocytes -> ILC2 + DC -> Th2 -> IL-4, IL-13 -> keratinocyte NF-kB -> TARC/CCL17 (additional Th2 recruitment) + CXCL8/IL-8 (neutrophils) -> cycle itchy. Chronification: NF-kB microglial sensitise (central pruritus) + NF-kB peripheral nerve -> neuropeptides SP, CGRP -> itch-scratch-barrier-break cycle. 6-Gingerol: keratinocyte NF-kB -40%, IL-4 response -28%, IL-13 -30%, TSLP reduced production, TARC -35%. GIMBER = Th2 amplifies via gut-skin axis: 35g sugar/100ml -> dysbiosis -> IgE sensitization -> systemic Th2 -> worsened dermatitis. INTI: 1.19g of sugar per 100ml.

Severe AD & keratinocyte NF-kB: the TSLP-Th2-IL-4/IL-13 axis

Atopic dermatitis is a Th2 disease orchestrated by keratinocyte NF-kB. The breakdown of the skin barrier (defective filaggrin, aggressive soaps, dry air) -> TSLP and IL-33 (alarmins) released by keratinocytes -> ILC2 and DC activation -> Th2 polarization -> IL-4/IL-13 -> keratinocyte NF-kB -> TARC/CCL17 -> additional Th2 recruitment -> vicious circle. Dupilumab (anti-IL-4/IL-13) is now the standard treatment for severe AD and confirms the central role of this axis.

Lane DA mechanism Gingerol
TSLP/IL-33 keratinocytes Alarmins -> ILC2 -> Th2 Keratinocyte NF-kB -40%
IL-4/IL-13 (Th2) Altered barrier + pruritus + TARC IL-4 -28%, IL-13 -30%
TARC/CCL17 Additional Th2 Recruitment TARC -35%
Gut-skin axis Dysbiosis -> IgE sensitization -> Th2 Microbiome (1.19g sugar)
GIMBER = Th2 amplifier through the gut-skin axis.
35g sugar/100ml -> dysbiosis (reduction of Bifidobacterium, Lactobacillus) -> intestinal permeability -> LPS + food antigens -> IgE sensitization -> systemic Th2 -> TARC -> cutaneous Th2 recruitment -> aggravated dermatitis.
INTI: 1.19g of sugar per 100ml. Microbiome preserved. Reduced IgE sensitization. Th2 less amplifies.
Medical note: INTI does not replace treatments for severe AD: dupilumab (anti-IL-4Ra), tralokinumab (anti-IL-13), baricitinib (JAK1/2 inhibitor), topical corticosteroids, intensive emollients. Severe AD significantly impacts quality of life -- specialized dermatological monitoring is essential. INTI contributes complementarily via the gut-skin axis and keratinocyte NF-kB.
Why is AD worse at night?

Three circadian reasons: (1) the cortisol-stress-adrenal-burnout">ginger cortisol-natural">ginger and cortisol (anti-inflammatory-science-usage">anti-inflammatory ginger) is at its lowest at night -> keratinocyte NF-kB is slowed down during the day but gets out of control at night; (2) body temperature increases at night -> vasodilation -> pruritus increases; (3) unconscious nocturnal scratching perpetuates barrier breakdown. In addition, nocturnal melatonin, normally anti-inflammatory, is paradoxically pro-pruritic in AD via the receptors melatonin in keratinocytes Management of nocturnal pruritus (sedative H1 antihistamine, low-dose SSRI) is crucial.

NRTI: Keratinocyte anti-NF-kB for AD

1.19g of sugar per 100ml | Keratinocyte NF-kB -40% | IL-4 -28% | TARC -35%

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