Nickel(II) sulphate-induced allergic contact dermatitis as experimental tool to investigate inflammatory pruritus in humans.

Allergic contact dermatitis is a leading cause of occupational skin disease, with nickel(II) sulphate representing one of the most prevalent contact allergies worldwide. Clinically, nickel-induced dermatitis is characterised by pronounced inflammation and intense pruritus. The functional role of endogenous mediators, structural neuronal changes, and molecular mediators contributing to the generation of itch in allergic contact dermatitis still needs to be investigated. We present nickel(II) sulphate-induced contact dermatitis as a mechanistic model to investigate pruritus under controlled conditions in humans. Thereby, we can combine and correlate clinical characterisation of nickel(II) sulphate contact dermatitis with psycho-physical, structural, and molecular analyses to identify inflammatory pathways, mediator profiles, and gene regulatory pathways involved in pruritus generation. By enabling the systematic characterisation of itch mechanisms at molecular, structural, and functional, levels, this approach provides a translational scope to advance our understanding of pruritogenic pathways and for developing targeted therapeutic strategies in allergic contact dermatitis.