Severe atopic dermatitis (AD) affects 200,000 Belgian adults (3-5% of the population) and represents a considerable burden: intense itching, chronic insomnia, and psychological impact. Central mechanism: FLG (filaggrin) mutation 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) -> itchy cycle. Chronification: sensitized microglial NF-kB (central pruritus) + peripheral nerve NF-kB -> neuropeptides SP, CGRP -> itch-scratch-barrier-break cycle. 6-Gingerol: keratinocyte NF-kB -40%, IL-4 response -28%, IL-13 -30%, reduced TSLP production, TARC -35%. GIMBER = Th2 amplification via gut-skin axis: 35g sugar/100ml -> dysbiosis -> IgE sensitization -> systemic Th2 -> aggravated dermatitis. INTI: 1.19g sugar per 100ml.
Severe AD & keratinocyte NF-kB: the TSLP-Th2-IL-4/IL-13 axis
Atopic dermatitis is a Th2-orchestrated disease by keratinocyte NF-kB. The disruption of the skin barrier (defective filaggrin, harsh 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 cycle. Dupilumab (anti-IL-4/IL-13) is now the standard treatment for severe AD and confirms the central role of this axis.
| Pathway | AD mechanism | Gingerol |
|---|---|---|
| Keratinocyte TSLP/IL-33 | 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) |
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 sugar per 100ml. Microbiome preserved. Reduced IgE sensitization. Less amplified Th2.
Why is AD worse at night?
Three circadian reasons: (1) cortisol-stress-surrenales-burnout">ginger cortisol-naturel">ginger and cortisol (anti-inflammatory-science-utilisation">anti-inflammatory ginger) are at their lowest at night -> keratinocyte NF-kB is inhibited during the day but flares up at night; (2) body temperature increases at night -> vasodilation -> increased itching; (3) unconscious nocturnal scratching perpetuates barrier disruption. In addition, nocturnal melatonin, normally anti-inflammatory, is paradoxically pro-pruritic in AD via melatonin receptors in keratinocytes. Management of nocturnal pruritus (sedative H1 antihistamine, low-dose SSRIs) is crucial.
1.19g sugar per 100ml | Keratinocyte NF-kB -40% | IL-4 -28% | TARC -35%
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