The role of airborne proteins in atopic dermatitis

Abstract

Atopic dermatitis is a common, chronic skin condition. A subpopulation of patients may have cutaneous exposure to common airborne proteins exacerbating their disease through direct proteolytic activity, direct activation of proteinase-activated receptor-2 itch receptors, and immunoglobulin E binding. The most common airborne proteins significant in atopic dermatitis include house dust mites, cockroach, pet dander, and multiple pollens. The literature on atopy patch testing, skin-prick testing, and specific IgE is mixed, with greater support for the use of atopy patch test. Patients with airborne proteins contributing to their disease typically have lesions predominately on air-exposed skin surfaces including the face, neck, and arms; a history of exacerbations after exposure to airborne proteins; severe disease resistant to conventional therapies; and concurrent asthma. Treatment strategies include airborne protein avoidance, removal of airborne proteins from the skin, and barrier repair. Further research is needed to establish the benefit of allergen-specific immunotherapy.

Figure 1

An overview of the cellular and molecular mechanisms through which airborne proteins aggravate barrier dysfunction and inflammation in atopic dermatitis patients. Airborne proteins cause increased local inflammation, increased itch sensation, and increased IgE sensitization through their proteolytic activity, their activation of PAR-2 receptors on keratinocytes and unmyelinated C fibers, and their ability to act as an allergen via Type I IgE-mediated hypersensitivity.

Figure 2

This demonstrates air-exposed atopic dermatitis in a 43-year-old man with a history of severe allergic rhinitis, asthma, and long-standing atopic dermatitis. At his initial presentation he reported intense nighttime itching and had failed multiple topical and systemic therapies for atopic dermatitis. His exam showed involvement primarily of the distal two-thirds of the arms, neck, and face. A diagnosis of airborne, protein-driven atopic dermatitis was made. Dust mite avoidance was initiated, along with barrier repair therapy with a ceramide-dominant moisturizer. Six weeks later, the patient reported that his skin was in the best condition he could recall in several decades.