Induction of atopic dermatitis by inhalation of house dust mite

Tupker, Ron A.; Monchy, J. G. R. De; Coenraads, Pieter Jan; Homan, Aafke; Meer, J. B. Van Der

doi:10.1016/s0091-6749(96)70259-2

Cited by 166 publications

(81 citation statements)

References 21 publications

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“…It is known that the route of allergen exposure is an important factor in the development of AD lesions. In some patients, contact of the skin with specific aeroallergens causes flares of AD [16], while in others inhalation of allergens results in the development or exacerbation of skin lesions [17]. In order to develop a cutaneous eosinophilic inflammation model in the present study, i.p.-primed mice were sensitized by the OVA skin application method.…”

Section: Discussionmentioning

confidence: 99%

Development of a novel Ag-specific immunotherapy using CpG oligodeoxynucleotides in a new, unique mouse cutaneous eosinophilic inflammation model

et al. 2005

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The number of patients with severe atopic dermatitis (AD) has been on the rise recently. We are therefore urgently in need of a treatment that can suppress Th2 cell-mediated responses in an Ag-specific fashion. Oligodeoxynucleotides (ODN)containing CpG motifs (CpG ODN) have been highlighted as immunomodulators that reduce Th2-mediated responses. To determine the effect of CpG ODN on Th2-mediated skin inflammation, we first developed a reproducible murine model of protein Ag-induced eosinophilic inflammation that is accompanied by epidermal acanthosis and increased serum IgE levels as seen in AD. In this model we found that treatment with CpG ODN during epicutaneous sensitization in previously i.p.-primed mice prevented the development of Th2-mediated responses. Furthermore, to evaluate the therapeutic effect of CpG ODN on established eosinophilic inflammation, mice were treated with a course of the immunotherapy at a skin site remote from the area of Ag application prior to the second 1-wk epicutaneous exposure to Ag. Therapeutic treatment with CpG ODN plus Ag, but not that with CpG ODN alone, could reverse the established eosinophilic inflammation. The presented results provide strong evidence for the feasibility of a novel Ag-specific immunomodulator to treat cutaneous eosinophilic inflammation such as that characteristically found in patients with severe AD.

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Section: Discussionmentioning

confidence: 99%

Development of a novel Ag-specific immunotherapy using CpG oligodeoxynucleotides in a new, unique mouse cutaneous eosinophilic inflammation model

et al. 2005

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“…Well-controlled studies have demonstrated that food allergens can exacerbate skin rashes in a subset of patients with AD (8). A role for inhaled allergens in AD is suggested by the observation that pruritus and eczematoid skin lesions develop in patients with AD after inhalation challenge with aeroallergens (9). Epicutaneous (EC) application of a number of inhalant allergens to normal skin sites elicits a positive reaction (10) and patch testing of abraded skin with mite extract results in an eczematous rash in patients with AD (11).…”

Section: Introductionmentioning

confidence: 99%

Epicutaneous sensitization with protein antigen induces localized allergic dermatitis and hyperresponsiveness to methacholine after single exposure to aerosolized antigen in mice.

Spergel

Mizoguchi²,

Brewer³

et al. 1998

J. Clin. Invest.

584

575

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Our understanding of the pathogenesis of atopic dermatitis (AD) and its relationship to asthma remains incomplete. Herein, we describe a murine model of epicutaneous (EC) sensitization to the protein allergen, chicken egg albumin, ovalbumin (OVA), which results in a rise in total and OVAspecific serum IgE and leads to the development of a dermatitis characterized by infiltration of CD3 ϩ T cells, eosinophils, and neutrophils and by local expression of mRNA for the cytokines IL-4, IL-5, and interferon-␥ . A single exposure of the EC sensitized mice to aerosolized OVA induced eosinophilia in the bronchoalveolar lavage fluid and airway hyperresponsiveness to intravenous methacholine as assessed by measurement of pulmonary dynamic compliance (C dyn ). These results suggest a possible role for EC exposure to antigen in atopic dermatitis and in the development of allergic asthma. (

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“…Airborne proteins may gain access to the body more easily through the bronchial mucous membranes than through the stratum corneum of the skin, because the stratum corneum does not allow salient penetration of substances with a molecular mass larger than ϳ500 Da. In fact, there is substantial evidence indicating that inhalation of an airborne allergen, the house dust mite, induces exacerbation of pre-existing skin exanthemas and/or new induction of erythemata (45). We dermatologists have underestimated the roles of the respiratory tract for the onset or maintenance of AD and for the induction of tracheal tolerance associated with allergy against airborne Ags.…”

Section: Discussionmentioning

confidence: 99%

TGF-β-Producing CD4+ Mediastinal Lymph Node Cells Obtained from Mice Tracheally Tolerized to Ovalbumin (OVA) Suppress Both Th1- and Th2-Induced Cutaneous Inflammatory Responses to OVA by Different Mechanisms

Terada¹,

Sano

Shirota

et al. 2001

The Journal of Immunology

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Advances in the treatment of allergic disorders require elucidation of the autoregulatory immune systems induced in averting detrimental inflammatory responses against invading foreign Ags. We previously reported that excessive Ags intruding through the airway mucosa induce a subset of regulatory CD4+ T cells secreting TGF-β in the regional mediastinal lymph nodes (MLNs), which inhibits Th2 cells and subsequent eosinophilic inflammation in the trachea. In the present experiments we examined whether and in what mechanisms TGF-β-secreting CD4+ T cells in the MLNs regulate Th cell-mediated skin inflammation using a previously established murine model. Th1 or Th2 cells injected s.c. into ear lobes of naive mice induced swelling, whereas the concomitant local injection of MLN cells suppressed the inflammation. The suppressor activities of MLN cells were markedly neutralized by anti-TGF-β mAb and were mimicked by rTGF-β. The MLN cell- and rTGF-β-induced inhibition was reversed by anti-IL-10 mAb significantly in Th1-induced inflammation and only partially in Th2-induced inflammation. rIL-10 reduced Th-induced ear swelling, although higher doses of rIL-10 were required in Th2-induced one. Thus, allergen-specific TGF-β-producing CD4+ T cells induced in the respiratory tract controlled cutaneous inflammatory responses by Th1 or Th2 cells either directly by TGF-β or indirectly through IL-10 induction. From a clinical standpoint, these observations might explain the mechanism of spontaneous regression in some patients with atopic dermatitis, which exhibits both Th1- and Th2-mediated skin inflammation in response to airborne protein Ags.

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Induction of atopic dermatitis by inhalation of house dust mite

Cited by 166 publications

References 21 publications

Development of a novel Ag-specific immunotherapy using CpG oligodeoxynucleotides in a new, unique mouse cutaneous eosinophilic inflammation model

Development of a novel Ag-specific immunotherapy using CpG oligodeoxynucleotides in a new, unique mouse cutaneous eosinophilic inflammation model

Epicutaneous sensitization with protein antigen induces localized allergic dermatitis and hyperresponsiveness to methacholine after single exposure to aerosolized antigen in mice.

TGF-β-Producing CD4+ Mediastinal Lymph Node Cells Obtained from Mice Tracheally Tolerized to Ovalbumin (OVA) Suppress Both Th1- and Th2-Induced Cutaneous Inflammatory Responses to OVA by Different Mechanisms

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