Recent insights into atopic dermatitis and implications for management of infectious complications

Atopic dermatitis (AD) is a common complex disease that frequently follows a chronic relapsing course and affects the quality of life of patients and families in a significant manner. New insights into the pathophysiology of AD point to an important role of structural abnormalities in the epidermis combined with immune dysregulation. Patients with AD have a unique predisposition to colonization or infection by a number of microbial organisms, most notably Staphylococcus aureus and herpes simplex virus. A multipronged approach directed at healing or protecting the skin barrier and addressing the immune dysregulation is necessary to improve the likelihood of successful outcomes.

Key words: Atopic dermatitis, filaggrin, epidermal barrier, Staphylococcus aureus, herpes simplex virus, superantigens, T regulatory cells, eczema herpeticum, antimicrobial peptides, probiotics

Abbreviations used: AD, Atopic dermatitis, ADVN, Atopic Dermatitis and Vaccinia Network, agr, Accessory gene regulator, AIP, Autoinducing peptide, CA, Community acquired, CLA, Cutaneous lymphocyte–associated antigen, EH, Eczema herpeticum, FLG, Filaggrin gene, FoxP3, Forkhead box protein 3, HBD, Human β-defensin, H4R, H4 histamine receptor, HSV, Herpes simplex virus, IVIG, Intravenous immunoglobulin, LTA, Lipoteichoic acid, MRSA, Methicillin-resistant Staphylococcus aureus, SAg, Superantigen, SEB, Staphylococcal enterotoxin B, TEWL, Transepidermal water loss, Treg, Regulatory T, VV, Vaccinia virus