Quantitative Assessment of Immediate Cutaneous Hypersensitivity in a Model of Genetic Predisposition to Atopy

Daser, Angelika; Bätjer, Nina; Kölsch, Uwe; Kötz, Karsten; Schmeling, Heinrike; Schou, C.; Renz, Harald

doi:10.1159/000024017

Cited by 13 publications

(8 citation statements)

References 6 publications

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“…Genetic variance of a candidate gene and proof of the functional relevance of these polymorphisms has been demonstrated in a study of immediate cutaneous hypersensitivity (ICHS) after sensitization with birch pollen extract [34]. The genome-wide linkage and gene analysis revealed the IL-5Rα chain (Il5ra) on chromosome 6 as a strong candidate gene [35].…”

Section: Linkage Of Atopy-related Phenotypes Of the Skinmentioning

confidence: 99%

Mouse Models for the Genetic Dissection of Atopy

Heinzmann

Daser

2002

Int Arch Allergy Immunol

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Atopic disorders are complex traits with a significant contribution of heritability. Several mouse models for atopic phenotypes such as allergen-induced and intrinsic asthma, atopic dermatitis and immediate cutaneous hypersensitivity have been used to systematically dissect the genetics of these diseases. Many of the chromosomal regions identified in genome-wide screens colocalize with linkage regions of autoimmune phenotypes suggesting common regulatory genes in combination (or addition) to disease-specific genes. Moreover, many of these regions correspond to regions found in the human system, thus strengthening the likelihood of a gene contributing to the phenotype. The role of individual candidate genes has been vigorously pursued in genetically modified mice by destruction or overexpression of the candidate gene. The complex interactions of multiple contributing genes may further be elucidated in randomly mutated mouse strains. Thus mouse models can contribute largely to the elucidation of disease genes.

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Section: Linkage Of Atopy-related Phenotypes Of the Skinmentioning

confidence: 99%

Mouse Models for the Genetic Dissection of Atopy

Heinzmann

Daser

2002

Int Arch Allergy Immunol

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“…Intracutaneous skin testing was performed as previously described (24). Briefly, abdominal skin was shaved, and 50 l of test solution was injected intradermally.…”

Section: Assessment Of Ichsmentioning

confidence: 99%

“…The following skin-test solutions were used: PBS as a negative control; Compound 48/80 (5 mg/ml; Sigma) as a positive control; and OVA at 0.5, 5, 50, and 100 g/ml (Sigma). After 15 min of development, the blue flair reactions were assessed as described (24). The skin tests were classified according to their intensity into three classes for each concentration applied.…”

Section: Assessment Of Ichsmentioning

confidence: 99%

Priming of Allergic Immune Responses by Repeated Ozone Exposure in Mice

Neuhaus-Steinmetz

Uffhausen

Herz

et al. 2000

Am J Respir Cell Mol Biol

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The effects of repeated ozone exposures on the development of immune responses toward ovalbumin (OVA) were investigated in BALB/c and C57BL/6 mice. Ozone exposures (180 to 500 microg/m(3); 4 h, three times/wk for 4 wk) were combined with a protocol of OVA-aerosol exposure (1% OVA). Immediate cutaneous hypersensitivity (ICHS) reactions and antibody titers were assessed in parallel to cytokine levels of bronchoalveolar lavage fluids. In BALB/c mice, ozone triggered a T-helper (Th)2-like response indicated by dose-dependent increases in total serum immunoglobulin (Ig) E (from 133 to 821 ng/ml), interleukin (IL)-4 (from 60 to 208 pg/ml), and IL-5 levels (from 43 to 356 pg/ml), and by the recruitment of eosinophils and lymphocytes into the airways. Ozone exposure (500 microg/m(3)) in parallel to OVA-aerosol exposure increased anti-OVA IgG(1) antibody titers by 80%, leukotrienes (C(4)/D(4)/E(4)) by 60%, and airway responsiveness (11.3 versus 7.2 mg/ml methacholine), and doubled the frequency of positive ICHS reactions. In C57BL/6 mice, only the combination of OVA and ozone exposure induced positive ICHS reactions, doubled anti-OVA IgG(1), and suppressed anti-OVA IgG(2a) (-64%) antibody titers. Ozone, therefore, shifted the immune responses to OVA toward a Th2-like pattern in both "IgE-high responder" (BALB/c) and "IgE-low responder" (C57BL/6) mice.

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“…Like AHR, there is strong evidence that atopy is in large part genetically determined in both human subjects and murine models of allergic disease [26][27][28][29]. Atopy, and its markers, are associated with a heightened risk of developing asthma in man [30,31].…”

Section: Atopymentioning

confidence: 99%

Toll-Like Receptors, Cytokines and the Immunotherapeutics of Asthma

Camateros

Moisan²,

Hénault³

et al. 2006

CPD

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Asthma is a complex disease caused by a poorly characterized set of genetic and environmental factors whose pathology is a result of immune dysregulation. Toll-like receptors are pathogen associated molecular pattern receptors expressed by many airway and pulmonary tissues as well as cells of the innate and adaptive immune system. Ligation of toll-like receptors can lead to a change in the expression levels of multiple inflammatory and anti-inflammatory mediators which are involved in the pathogenesis of asthma. These ligands and their receptors are therefore prime candidates in the search for immunotherapeutic treatments of asthma. The use of murine models of allergic asthma as tools for the genetic dissection of this disease should allow the molecular mechanisms underlying asthma to be identified and possibly used as further immunotherapeutic targets.

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Quantitative Assessment of Immediate Cutaneous Hypersensitivity in a Model of Genetic Predisposition to Atopy

Cited by 13 publications

References 6 publications

Mouse Models for the Genetic Dissection of Atopy

Mouse Models for the Genetic Dissection of Atopy

Priming of Allergic Immune Responses by Repeated Ozone Exposure in Mice

Toll-Like Receptors, Cytokines and the Immunotherapeutics of Asthma

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