Fulvic Acid Attenuates Atopic Dermatitis by Downregulating CCL17/22
in-vitro Grade C 2023 Open access
Key Findings
- FA reduces CCL17 (TARC) and CCL22 (MDC) expression in TNF-α/IFN-γ-stimulated HaCaT keratinocytes
- FA inhibits CCL17 and CCL22 production by deactivating p38 MAPK and JNK signaling pathways
- Dose-dependent inhibition: 200 and 500 μg/mL FA reduced mRNA of TNF-α, IL-6, CCL2, CCL17, CCL22
- DNCB-induced AD mouse model: topical FA reduced ear thickness, erythema, edema, and desquamation
- FA dose-dependently reduced serum CCL17 and CCL22 levels in AD mice
- Higher dose FA (500 μg/mL) showed stronger therapeutic effect than lower dose (200 μg/mL)
- ICC confirmed FA decreased CCL17 and CCL22 protein expression in stimulated HaCaT cells
Combined in vitro and in vivo study demonstrating fulvic acid’s mechanism of action in atopic dermatitis. In keratinocyte cell culture, FA inhibited CCL17/CCL22 chemokine expression via p38 MAPK and JNK pathway deactivation. These chemokines are key drivers of Th2 cell recruitment to AD lesions. In the DNCB-induced AD mouse model, topical FA dose-dependently reduced clinical symptoms (ear thickness, redness, scaling) and serum chemokine levels. This is one of the most mechanistically detailed studies of FA in dermatological application, identifying specific signaling pathways rather than just observing effects.
fulvic-acidatopic-dermatitisCCL17CCL22MAPKJNKkeratinocytesmouse-modeldose-dependent