Dermatitis, or skin inflammation, can have many causes and forms.

One form is atopic dermatitis, an immune-mediated skin inflammation where pruritus is the primary symptom and skin lesions can range from mild erythema to severe lichenification, or scaling. It is quite commonly found in children and can pose an increased risk for developing other conditions like asthma. Contact dermatitis is another form caused by irritants or allergens. Common irritants and allergens can be water, detergents, friction, nickel, perfume, or preservatives. Skin lesions range from erythema to blistering and ulceration, occurring where the skin was exposed to the irritant or allergen. Seborrheic dermatitis targets areas that are populated with sebaceous glands such as the face and scalp, causing pruritus and dandruff. Other forms may present skin inflammation as systemic or localized. They may have autoimmune origins, can be due to an infection, or may be secondary to another disease process.

While not contagious or life-threatening, dermatitis can affect quality of life depending on the severity. Treatments are varied, depending on the type of dermatitis and range from avoiding the irritant or allergen to the administration of steroids, emollients, or chemotherapy.

Dermatitis affects one in every five people at some point in their lives. The incidence of dermatitis is high in developed countries, but worldwide, incidence is increasing. In America, there are approximately 31.6 million people with atopic dermatitis, with at least 17.8 million suffering from moderate to severe forms. Three percent of US adults need systemic therapy for moderate to severe atopic dermatitis. Currently, common treatments comprise of moisturizers for milder cases and agents like topical corticosteroids, calcineurin inhibitors, and antimicrobials are used for more moderate to severe cases.

Although there are a variety of treatments, there are large unmet needs for treatment of patients with atopic dermatitis. The reason for this discrepancy is because of an incomplete understanding of the disease. Further research is needed to identify specific causes, as well as develop treatments that can target these specific causes and inhibit chronic inflammation. Atopic dermatitis alone has a global market, and is forecasted to increase from $3.9 billion in 2012 to $5.6 billion in 2022. Incidence is also expected to increase worldwide and as the incidence increases, the present unmet need for effective therapies will increase as well.

Pharma Models LLC offers a variety of different models of dermatitis. The noninvasive mouse ear swelling test (MEST) is commonly used to study delayed-type contact hypersensitivity (CHS) seen in contact dermatitis. Induction is via topical sensitization on the shaved abdomen or back of BALB/C mice with dinitrochlorobenzene (DNCB), fluorescein isothiocyanate (FITC), or oxazolone. Five days after induction, the ears are topically challenged with the same chemical used at induction. Ear swelling is then measured at a predetermined time point. We also offer a primary allergic contact dermatitis (ACD) model, where murine ears are painted once with FITC or 1-fluoro-2,4-dinitrobenzene (DNFB).

Chemically induced CHS is a commonly used mouse model for studying dermatitis. Mechanistically, chemicals like DNCB, FITC, oxazolone, and DNFB complex with skin proteins to form covalent conjugates that function as immunogens, which are then internalized by local APCs (Langerhans cells, dermal dendritic cells, macrophages), processed, and presented to T cells for activation. BALB/C mice are painted with the chemical on their shaved backs or abdomens, then are challenged on one of the ears five days after induction. The thickness of the ears are then measured 24 hours later. Ear and skin tissues are then collected to quantitatively assess immunologic response.

The primary allergic contact dermatitis model (ACD) is also known as irritant contact dermatitis or primary CHS and can be studied by using a one-step method. C57BL/6 mice have their ears painted with urushiol, DNFB, FITC or DNCB. The lesions produced are indistinguishable from those present in conventional ACD.