**2. Allergic contact dermatitis**

Most of our knowledge on the pathophysiology of contact dermatitis is derived from murine models of Allergic Contact Dermatitis (ACD), a T cell mediated delayed-type hypersensitivity reaction also referred to as contact hypersensitivity (CHS). In this model, skin inflammation is induced by topical application on the epidermis of sensitizing chemical agents which act as haptens (Eisen et al., 1952).

Haptens can be defined as low molecular weight chemicals which are not immunogenic by themselves and that generate new antigenic determinants by binding to epidermal proteins. The reactive haptens commonly employed for ACD induction in murine models include oxazolone (OX), dinitrochlorobenzene (DNCB), dinitrofluorobenzene (DNFB), trinitrochlorobenzene (TNCB), picryl chloride (PI), and fluorescein isothiocyanate (FITC).

Such widely employed haptens are all strong contact allergens exhibiting high proinflammatory capacities which therefore differ from the vast majority of chemicals

Animal Models of Contact Dermatitis 25

Fig. 1. Schematic representation of the pathophysiology of the different phases of allergic contact dermatitis. (A) the sensitization phase (B) the elicitation phase (C) the resolution

Experimental protocol for ACD induction is graphically summarized in Figure 2. For sensitization, mice are painted at day 0 on the shaved back (or abdomen) with 100 μl of DNFB 0.5% in a 4:1 mixture of acetone and olive oil. Mice are challenged 6 days later by application of 20 μl DNFB 0.2% in olive oil (10 μl to each side of one ear). Ear thickness is measured with a digital calliper before challenge and at 24-48 hours after treatment. Ear swelling is calculated by subtracting the value recorded for vehicle-control ear from the hapten-applied ear. Histological examination can be performed in order to confirm changes in ear thickness and to quantify cellular infiltration. Moreover, lymphocytes infiltrating

phase.

**2.2 Experimental protocol** 

responsible for human ACD. Importantly recent studies have reproduced the conclusions drawn with strong allergens by using weak haptens (Vocanson et al., 2006; Vocanson et al., 2009) which are more close to those encountered in clinical practice.
