Atopic Dermatitis in 2008

Abstract

Atopic dermatitis (also termed atopic eczema and infantile eczema), a chronic, itchy, inflammatory skin disease that sets on at infancy or early childhood, is observed with increasing prevalence around the world, particularly in developed nations. Although sufficient evidences are not yet available to define it as a classical autoimmune disease, autoantigens have been identified. Investigations of atopic dermatitis in human patients and animal models suggest that this disease is initiated, maintained and perpetuated by the actions of cytokines, chemokines, T cells, antigen-presenting cells and other inflammatory cells; there is also evidence of skin barrier defect and angiogenesis. Recent identification of mutations of the epidermal barrier protein filaggrin (encoded by FLG), present in about 9% of people of European origin, with 70% of individuals homozygous or compound heterozygous for FLG null alleles developing atopic dermatitis, provides a strong link between a defect of the epidermal barrier that allows easy penetration of pathogen/allergen through the skin and a systemic hyperactive immune response to the penetrated pathogen/allergen. The newly introduced concept of 'intrinsic' and 'extrinsic' atopic dermatitis has fueled the debate among academic dermatologists as to how 'atopic' atopic dermatitis should be defined. Some recent advancements on the management options for atopic dermatitis are also discussed.

Evaluation of Nisin F in the Treatment of Subcutaneous Skin Infections, as Monitored by Using a Bioluminescent Strain of Staphylococcus aureus

“…3d). Atopic dermatitis, although not yet defined as an autoimmune disease, is initiated and maintained by the actions of inflammatory cells such as cytokines, chemokines and T-cells [5]. Mice treated with nisin (both the infected and non-infected groups) had a higher number of polymorphonuclear cells in the dermal stromas of the skin tissue.…”

Interleukin-4 Downregulation of Involucrin Expression in Human Epidermal Keratinocytes Involves Stat6 Sequestration of the Coactivator CREB-Binding Protein

“…Although the etiology and pathogenesis of AD are not fully understood, it is generally accepted that skin barrier defects play an essential role (Chan 2008;Schittek 2011;Simon and Kernland Lang 2011). Genetically, several skin barrier protein polymorphisms have been linked to AD (Henry and others 2011;Lan and others 2011;Knuppel and others 2012;Margolis and others 2012;Paternoster and others 2012;Ring and others 2012).…”

Interleukin-8 Content in the Stratum Corneum as an Indicator of the Severity of Inflammation in the Lesions of Atopic Dermatitis

“…Recent studies have provided insights into the underlying immunologic mechanisms, suggesting an amplification cycle of atopic skin inflammation [2]. Investigations of AD in patients and animal models suggest that this disease is initiated, maintained and perpetuated by the actions of various inflammatory cytokines and growth factors secreted by keratinocytes, antigen-presenting dendritic cells, T cells and other inflammatory cells, although there is also evidence of a skin barrier defect [3]. These cytokines and growth factors regulate not only the immune and inflammatory responses but also the proliferation and differentiation of skin components [4], thus these components can reflect inflammatory conditions of lesional skin in AD.…”