Validated safety predictions of airway responses to house dust mite in asthma

Ravensberg, A. Janneke; Rensen, Elizabeth L J van; Grootendorst, Diana C.; Kluijver, Josephine de; Diamant, Zuzana; Ricciardolo, Fabio Luigi Massimo; Sterk, Peter J.

doi:10.1111/j.1365-2222.2006.02617.x

Cited by 16 publications

(12 citation statements)

References 29 publications

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“…As ovalbumin exposure models require artificial sensitization [30], they may lead to allergen tolerance [31], and are not reflective of clinically relevant allergens [32–34], we sought to examine whether up‐regulation of the GABAergic signalling system was conserved for more relevant allergens. Using a model of acute HDM exposure that requires no artificial sensitization, results in no allergen tolerance [22, 33, 35], and is of clinical relevance [36], we demonstrate that GABAergic up‐regulation in airway epithelium is conserved among two common models of allergen exposure.…”

Section: Discussionsupporting

confidence: 92%

The role of interleukin‐4Rα in the induction of glutamic acid decarboxylase in airway epithelium following acute house dust mite exposure

Hirota

Budelsky

Smith

et al. 2010

Clin Experimental Allergy

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Background Asthma is a disease characterized by airway inflammation, remodelling and dysfunction. Airway inflammation contributes to remodelling, a term that is used to describe structural changes including goblet cell metaplasia (GCM), matrix deposition, and smooth muscle hyperplasia/hypertrophy. GCM has been implicated in asthma mortality by contributing to mucus plugs and leading to asphyxiation. In animal models, this process is highly dependent on IL-13. Recently, we have described an IL-13-dependent up-regulation of a GABAergic signalling system in airway epithelium that contributes to GCM. The mechanism by which IL-13 up-regulates GABA signalling in airway epithelium is unknown. Objectives To test the hypothesis that IL-4Ralpha signalling is required for allergen induced up-regulation of GABAergic signalling and GCM. Methods BALB/c mice were exposed to an acute house dust mite (HDM) protocol and received vehicle, anti-IL-4Ralpha-monoclonal antibody, or control antibody. Outcomes included airway responses to inhaled methacholine (MCh), histology for eosinophilia and GCM, phosphorylated STAT6 levels using immunohistochemistry and immunoblot, and glutamic acid decarboxylase (GAD) 65/67 and GABA(A)beta(2/3) receptor subunit expression using confocal microscopy. Results Acute HDM exposure resulted in increased airway responses to MCh, lung eosinophilia, STAT6 phosphorylation, elevations in GAD65/67 and GABA(A)beta(2/3) receptor expression, and GCM that were inhibited with anti-IL-4Ralpha-monoclonal treatment. Control antibody had no effect. Conclusion The IL-4Ralpha is required for allergen-induced up-regulation of a GABAergic system in airway epithelium implicated in GCM following acute HDM exposure.

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Section: Discussionsupporting

confidence: 92%

The role of interleukin‐4Rα in the induction of glutamic acid decarboxylase in airway epithelium following acute house dust mite exposure

Hirota

Budelsky

Smith

et al. 2010

Clin Experimental Allergy

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“…In former studies, the predictive value of the SPT had been predominantly investigated . In children, a wheal size of ≥4.5 mm showed a sensitivity of 75% and a specificity of 86% to predict an EAR (AUC 0.85) .…”

Section: Discussionmentioning

confidence: 99%

“…In adults, a positive SPT (wheal size 3 mm) failed to discriminate between challenge‐positive and challenge‐negative patients . In HDM allergies, the skin sensitivity did not significantly contribute to the prediction of an EAR . We used the SPT only to screen the patients and focused on the allergen‐specific IgE.…”

Section: Discussionmentioning

confidence: 99%

Bronchial allergen challenges in children – safety and predictors

Schulze

Reinmüller

Herrmann

et al. 2013

Pediatric Allergy Immunology

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“…Serial twofold dilutions were prepared from standardized stock allergen (cat, 100 IR/mL, Stallergenes, Antony, France) and diluted in normal saline. Starting concentration for inhalation was determined by mathematical prediction of allergen PC 20 using the skin tests end‐point and methacholine PD 20 FEV 1 [16]. Increasing doses of allergen were administered by means of a breath‐activated dosimeter (Mefar MB3; Markos, Brescia, Italy) set to deliver 10 μL of solution during a deep breath until a decrease in FEV 1 of at least 20% was observed.…”

Section: Methodsmentioning

confidence: 99%

Oxidative stress and airway inflammation after allergen challenge evaluated by exhaled breath condensate analysis

Brussino¹,

Badiu²,

Sciascia³

et al. 2010

Clin Experimental Allergy

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The increase in EBC 8-isoprostane observed after allergen challenge indicates that allergen exposure increases airway oxidative stress in allergic asthma. The strict correlation between cys-LTs and 8-isoprostane underlines the relationship between allergic inflammation and oxidative stress. A shift of arachidonic acid metabolism towards lipoxygenase pathway is induced by the allergen challenge. Airway oxidative stress occurs after allergen challenge even in patients with mild intermittent allergic asthma.

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Validated safety predictions of airway responses to house dust mite in asthma

Cited by 16 publications

References 29 publications

The role of interleukin‐4Rα in the induction of glutamic acid decarboxylase in airway epithelium following acute house dust mite exposure

The role of interleukin‐4Rα in the induction of glutamic acid decarboxylase in airway epithelium following acute house dust mite exposure

Bronchial allergen challenges in children – safety and predictors

Oxidative stress and airway inflammation after allergen challenge evaluated by exhaled breath condensate analysis

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