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Summary Atopic dermatitis is a chronic inflammatory skin disease that affects 10–20% of the population. Linkage of atopy, asthma, allergic rhinitis, and total serum IgE levels to several different chromosomal regions have been described extensively, but little is known about the genetic control of atopic dermatitis. We tested for the association and linkage between atopic dermatitis and five chromosomal regions: 5q31–33, 6p21.3, 12q15–24.1, 13q12–31, and 14q11.2/14q32.1–32.3. Marker analysis was performed in two Caucasian populations: (i) 192 unrelated German children with atopic dermatitis and 59 non-atopic children from a German birth cohort study (MAS'90), parental DNA was tested in 77 of 192 children with atopic dermatitis; (ii) 40 Swedish families with at least one family member with atopic dermatitis selected from the International Study of Asthma and Allergy in Children. Evidence for linkage and allelic association for atopic dermatitis was observed for markers on chromosome 13q12–14 and 5q31–33. [ABSTRACT FROM AUTHOR]

SummaryChronic inflammatory conditions of human skin, such as prurigo lesions of atopic dermatitis, are characterized clinically by intense pruritus and histologically by increased innervation. Regulation of skin innervation is thought to depend on neurotrophic factors. In this study, human skin cells were identified as a source of neurotrophins. Cultured keratinocytes expressed neurotrophin-4, whereas dermal fibroblasts expressed neurotrophin-3. In vitro stimulation with interferon-γ, a marker cytokine for atopic eczema, induced keratinocyte neurotrophin-4 production, which was able to support growth of a neuroglioblastoma-derived cell line. In vivo, immunohistochemistry of human skin for neurotrophins showed neurotrophin-4 staining in the epidermal layer and neurotrophin-3 staining in the dermal compartment. Neurotrophin-4 but not neurotrophin-3 expression was markedly increased in interferon-γ-injected skin. Prurigo lesions of atopic dermatitis skin were characterized by intense epidermal staining for neurotrophin-4, suggesting a pathophysiologic role for this neurotrophin in the increased innervation characteristic for these skin lesions. This study demonstrates differential expression and regulation of neurotrophins in human skin. It also identifies keratinocyte-derived neurotrophin-4 as a possible link between the immune and the nerve system of human skin. [ABSTRACT FROM AUTHOR]

Objectives: Prevalence studies of atopic diseases such as atopic dermatitis, hay fever and allergic asthma have mostly been performed in children. Studies in the adult population are still rare.We estimated the lifetime prevalence of atopic diseases in an elderly population in Saarland, Germany, and determined the association between the duration of school education (as a proxy measure of socio-economic status) and atopic diseases. Family history and size of residence with respect to atopic diseases have also been examined. Methods: This study was conducted between June 2000 and December 2002 in the State of Saarland, Germany. 9961 participants aged 50 to 75 years were recruited by their general practitioner. All filled out a standardized questionnaire and reported whether a physician ever had diagnosed an atopic disease (hay fever, atopic dermatitis or asthma). Results: Overall, 9949 subjects (mean age 62 yrs., 45 % male) were included in this analysis. The lifetime prevalence for asthma, atopic dermatitis and hay fever was 5.5%, 4.3% and 8.3%, respectively. Duration of school education (≤9 years, 10–11 years, >11 years) was strongly associated with atopic dermatitis and hay fever, but only tentatively with asthma. With increasing duration of school education the prevalence of atopic dermatitis (3.7%, 5.7%, 6.8%; P trend <.0001) and hay fever (7.2%, 11.2%, 12.8%; P trend <.0001) increased continuously. Conclusions: The lifetime prevalence for atopic dermatitis is considerably lower in the elderly compared to recent studies on prevalence among children and adolescents. Adults with a longer duration of school education appeared to have a higher risk for atopic diseases. [ABSTRACT FROM AUTHOR]

Psoriasis vulgaris and atopic dermatitis share a number of features such as chronic cutaneous inflammation and disturbed epidermal barrier function. Genome-wide scans have revealed a conspicuous overlap of susceptibility loci for both diseases involving chromosomal regions 1q21, 3q21, 17q25, and 20p12. Recently, two loss-of-function variants in the gene encoding filaggrin at 1q21 were shown to be strongly associated with atopic dermatitis. In view of a possible genetic overlap of the two skin diseases, we investigated 375 patients suffering from psoriasis vulgaris, 375 patients with psoriatic arthritis, and 376 control probands. Moreover we directly studied expression of filaggrin in 10 patients suffering from psoriasis vulgaris. Our immunohistochemical analysis revealed a checkered pattern with alternating positive broadened or almost absent filaggrin expression. However, no association was found for the two variants of filaggrin (FLG). We conclude that despite a markedly altered filaggrin expression in psoriatic skin, loss-of-function variants of the FLG gene are neither associated with psoriasis vulgaris nor with psoriatic arthritis. The abnormal staining might reflect the altered epidermal differentiation. Our findings imply that the genetic background underlying the epidermal barrier defect in psoriasis is distinct from that found in atopic dermatitis.Journal of Investigative Dermatology (2007) 127, 1367–1370. doi:10.1038/sj.jid.5700720; published online 25 January 2007 [ABSTRACT FROM AUTHOR]