Atopic dermatitis

Rudikoff, Donald; Lebwohl, Mark

doi:10.1016/s0140-6736(97)12082-7

Cited by 231 publications

(220 citation statements)

References 67 publications

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“…These observations in control NC mice were consistent with several previous reports that the Th2-mediated immune response is probably responsible for the development of skin lesions in NC mice (11,12,14,27). In many AD patients increased Th2 cytokines and serum IgE levels are regarded as a specific feature reflecting the development of disease (3)(4)(5)(6)28). These previous findings suggest that the NC strain would be a useful animal model for human AD (11).…”

Section: Discussionsupporting

confidence: 91%

“…Most patients have increased serum levels of IgE Ab against many kinds of allergens (2). Evidence suggests that the development and pathogenesis of AD are associated with immunological abnormalities, such as type I allergic reaction (3)(4)(5)(6). However, for many years controversy has surrounded the contribution of allergic or IgE-mediated hypersensitivity reactions to the pathogenesis of AD (7), because in some chronic AD skin lesions the development of AD appears to be independent of plasma IgE levels, but correlates with a significant increase in the number of cells expressing the Th1 cytokine, IFN-␥ (8 -10).…”

Section: Development Of Atopic Dermatitis-like Skin Lesions In Stat6-mentioning

confidence: 99%

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Development of Atopic Dermatitis-Like Skin Lesions in STAT6-Deficient NC/Nga Mice

Yagi

Nagai

Iigo

et al. 2002

The Journal of Immunology

121

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Atopic dermatitis (AD) is a pruritic inflammatory skin disease characterized by elevation of plasma levels of total IgE, infiltration of mast cells and eosinophils, and the expression of cytokines by Th2 T cells. However, the role of Th2 cells in the pathogenesis of AD is not fully understood. In this study we examined the NC/Nga (NC) mouse model of AD and established STAT6-deficient (SATA6−/−) NC mice to investigate the relevance of IL-4-mediated immune responses. Surprisingly, these mice elicited AD-like skin lesions at equivalent frequency and time of onset compared with normal NC littermates. Histological features of the lesion in STAT6−/− NC mice fulfilled the criteria for the pathogenesis of AD, although these mice fail to produce IgE and Th2 cytokines. The lymph nodes proximal to the regions of skin that developed lesions exhibited massive enlargement elicited by the accumulation of activated IFN-γ-secreting T cells. Moreover, caspase I, IL-18, IL-12, and IFN-γ are found to be highly expressed at the skin lesion, occurring simultaneously with elevation of eotaxin 2 and CCR3 expression. Therefore, the Th2-mediated immune response is not necessary for the development of AD-like skin disease in NC mice. The skin microenvironment that favored IFN-γ production tightly correlates with the skin disease in NC mice through the infiltration of eosinophils.

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Section: Discussionsupporting

confidence: 91%

Section: Development Of Atopic Dermatitis-like Skin Lesions In Stat6-mentioning

confidence: 99%

Development of Atopic Dermatitis-Like Skin Lesions in STAT6-Deficient NC/Nga Mice

Yagi

Nagai

Iigo

et al. 2002

The Journal of Immunology

121

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“…Many patients have elevated serum levels of immunoglobulin E (IgE) against many kinds of allergens, such as mites and dust. It has been well established that such allergens can trigger or exacerbate AD (Rudikoff and Lebwohl, 1998).…”

Section: Introductionmentioning

confidence: 99%

Psychological Stress can Trigger Atopic Dermatitis in NC/Nga Mice: An Inhibitory Effect of Corticotropin-Releasing Factor

Amano

Negishi

Akiyama

et al. 2007

Neuropsychopharmacol

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Atopic dermatitis (AD) is one of the most common inflammatory diseases of the skin and is usually associated with a family history of atopic diathesis. It has been well established that many environmental or psychological factors aggravate AD. However, it is not clear whether psychological stress by itself can trigger AD. We examined the effect of psychological stress on the onset of AD, using an animal model, the NC/Nga mouse. The animals were exposed to the water avoidance stress (WAS) test to induce psychological stress. Additionally, we examined how corticotropin-releasing factor (CRF) affected the development of AD induced by psychological stress. Under specific pathogen-free (SPF) conditions, NC/Nga mice did not develop AD-like skin lesions. In contrast, NC/Nga mice exposed to psychological stress developed AD-like skin lesions along with elevated levels of serum immunoglobulin E even when kept under SPF conditions. The AD-like skin lesions induced by WAS were completely blocked by pretreating the animals with CRF. Our data indicate that a psychological factor is capable of eliciting AD-like skin lesions in NC/Nga mice. It is possible that the inhibitory effect of CRF may be mediated by the functional modification of various cells that have CRF receptors.

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“…1,2 The skin lesions of AD patients are characterized by the presence of an inflammatory infiltrate consisting of T lymphocytes, monocytes/macrophages, eosinophils, and mast cells. 3,4 These cells are involved in the pathogenesis and development of AD through the release of various cytokines and chemokines including IL-4, IL-5, IL-10, IL-13, 5 GM-CSF, 6 and RANTES (regulated upon activation, normal T expressed and secreted).…”

Section: Introductionmentioning

confidence: 99%

“…In addition, the level of IgE in the blood gradually increases to high levels. 2 Although these immunological, histological, and biochemical changes of NC/Nga mice kept in conventional conditions resemble human AD, 14 the mechanisms are not fully clear yet.…”

Section: Introductionmentioning

confidence: 99%

Improvement of dermatitis by iontophoretically delivered antisense oligonucleotides for interleukin-10 in NC/Nga mice

et al. 2004

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IL-10 is overexpressed in skin lesions of atopic dermatitis (AD) patients and believed to be an important factor in the pathogenesis of the disease. Thus the regulation of IL-10 production is a potential solution for immunotherapeutic intervention in AD. We examined the topical delivery of an antisense oligonucleotide for mouse IL-10 (AS6) and the therapeutic effect on the skin lesions of NC/Nga mice, a human AD model. Using an iontophoresis system, about 30% of the applied dose of AS6 penetrated the skin and was distributed in the epidermis and upper dermis. Topically delivered AS6 decreased the levels of mRNA and protein of IL-10 in the lesions of NC/Nga mice, with no effect on IL-4 levels. The dorsal lesions of NC/Nga mice disappeared with repeated topical application of AS6. Topically delivered AS6 showed an inhibitory effect on the production of IL-10 in the skin lesions of NC/Nga mice and had a therapeutic effect on the established dermatitis.

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Atopic dermatitis

Cited by 231 publications

References 67 publications

Development of Atopic Dermatitis-Like Skin Lesions in STAT6-Deficient NC/Nga Mice

Development of Atopic Dermatitis-Like Skin Lesions in STAT6-Deficient NC/Nga Mice

Psychological Stress can Trigger Atopic Dermatitis in NC/Nga Mice: An Inhibitory Effect of Corticotropin-Releasing Factor

Improvement of dermatitis by iontophoretically delivered antisense oligonucleotides for interleukin-10 in NC/Nga mice

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