Disease relevance of Dermatitis, Atopic

• Spontaneous release of histamine from basophils and histamine-releasing factor in patients with atopic dermatitis and food hypersensitivity [1].
• Atopic dermatitis is a chronic inflammatory skin disease associated with cutaneous hyperreactivity to environmental triggers and is often the first step in the atopic march that results in asthma and allergic rhinitis [2].
• In the current study, we investigated whether Staphylococcus aureus grown from affected skin of atopic dermatitis (AD) patients secreted identifiable toxins that could act as allergens to induce IgE-mediated basophil histamine release [3].
• Several immunological disorders including allergic rhinitis, bronchial asthma, atopic dermatitis, food allergies, urticaria, nonhereditary angioedema, systemic anaphylaxis, and allergic conjunctivitis are associated with a positive family history, and share a positive response in the Prausnitz-Kuster (wheal and flare) reaction [4].
• Perinatal administration of the probiotic Lactobacillus rhamnosus strain GG (ATCC 53103), reduces incidence of atopic eczema in at-risk children during the first 2 years of life (infancy) [5].

Psychiatry related information on Dermatitis, Atopic

• Sleep disorders in patients with asthma, atopic dermatitis, and allergic rhinitis [6].

High impact information on Dermatitis, Atopic

• Common loss-of-function variants of the epidermal barrier protein filaggrin are a major predisposing factor for atopic dermatitis [7].
• Atopic or immunoglobulin E (IgE)-mediated diseases include the common disorders of asthma, atopic dermatitis and allergic rhinitis [8].
• Genetic linkage of childhood atopic dermatitis to psoriasis susceptibility loci [9].
• Along with asthma and allergic rhinitis, atopic dermatitis is an important manifestation of atopy that is characterized by the formation of allergy antibodies (IgE) to environmental allergens [10].
• Increased plasma histamine concentrations after food challenges in children with atopic dermatitis [11].

Chemical compound and disease context of Dermatitis, Atopic

• Double-blind controlled trial of effect of housedust-mite allergen avoidance on atopic dermatitis [12].
• The frequency of atopic eczema in the probiotic group was half that of the placebo group (15/64 [23%] vs 31/68 [46%]; relative risk 0.51 [95% CI 0.32-0.84]) [13].
• Heparin-like activity, atopic eczema, and contact dermatitis [14].
• Retinoid X receptor ablation in adult mouse keratinocytes generates an atopic dermatitis triggered by thymic stromal lymphopoietin [15].
• Consequently, hPGD(2)S-derived cyclopentenone PGs may protect against inflammatory diseases, where T lymphocytes play a pathogenic role, as in rheumatoid arthritis, atopic eczema, and chronic rejection [16].

Biological context of Dermatitis, Atopic

• Our findings indicate that distinct genetic factors contribute to susceptibility to atopic dermatitis and that the study of this disease opens new avenues to dissect the genetics of atopy [10].
• Molecular evolution of the human immunoglobulin E response: high incidence of shared mutations and clonal relatedness among epsilon VH5 transcripts from three unrelated patients with atopic dermatitis [17].
• We have analyzed the nucleotide sequences of 19 epsilon VH5 transcripts derived from in vivo isotype switched peripheral blood B cells of three patients with atopic dermatitis [17].
• Chromosome 11q13 and atopy underlying atopic eczema [18].
• Association of the IL12RB1 promoter polymorphisms with increased risk of atopic dermatitis and other allergic phenotypes [19].

Anatomical context of Dermatitis, Atopic

• TSLP is highly expressed by keratinocytes in skin lesions of patients with atopic dermatitis and is associated with dendritic cell activation in situ, suggesting that TSLP might be a master switch for allergic inflammation at the epithelial cell-dendritic cell interface [20].
• However, the sustained chronic skin inflammation that characterizes atopic dermatitis is likely to result from a local expansion of allergen-specific T helper type 2 cells that produce interleukin-4 and interleukin-5 and the concomitant infiltration of eosinophils [21].
• The unique C-terminal extension was crucial for its plasma membrane localization and optimal cellular functions. sPLA(2)-IIF expression was increased in various tissues from lipopolysaccharide-treated mice and in ears of mice with experimental atopic dermatitis [22].
• Prostaglandin E2 control of T cell cytokine production is functionally related to the reduced lymphocyte proliferation in atopic dermatitis [23].
• IgG-, IgA-, and IgE-induced release of leukotriene C4 by monocytes isolated from patients with atopic dermatitis [24].

Gene context of Dermatitis, Atopic

• Genes implicated so far in atopic dermatitis are SPINK5, FcepsilonRI-beta and PHF11 [25].
• Interleukin-13 (IL-13), a predominantly Th2-derived cytokine, appears to play a central pathological role in asthma, atopic dermatitis, allergic rhinitis, some parasitic infections, and cancer [26].
• Enhanced expression of B7.2 (CD86) in patients with atopic dermatitis: a potential role in the modulation of IgE synthesis [27].
• In vivo, topical exposure to the relevant allergen or the superantigen staphylococcal enterotoxin B, resulted in a significant induction of CCL18 in atopic dermatitis patients [28].
• CCL1 serum levels of atopic dermatitis patients are significantly higher than levels in healthy individuals [29].

Analytical, diagnostic and therapeutic context of Dermatitis, Atopic

• Double-blind, controlled, crossover study of cyclosporin in adults with severe refractory atopic dermatitis [30].
• We therefore renormalized skin biopsy cDNA according to the level of beta-actin PCR product, as a marker of total cellular mRNA, and found by PCR that IL-10 was nevertheless greatest in atopic dermatitis subjects [31].
• Gel filtration studies indicated that the anti-IgE autoantibody in sera from atopic dermatitis was mainly present in the form of an immune complex with self IgE [32].
• OBJECTIVE: The study was designed to evaluate the atopy patch test (APT) and the late-phase reaction (LPR) after intracutaneous allergen injection as models for the study of allergic inflammation in atopic eczema [33].
• Systemic corticosteroidal agents, certain antihistiminic agents, systemic cyclosporin, and phototherapy have proven value in treating patients with atopic dermatitis [34].

References