Sentence examples for models of allergen from inspiring English sources

Recently established murine models of allergen sensitisation followed by long term allergen challenges do not only lead to impaired lung function (similar to short term challenge models) but also to airway wall remodelling, a feature typical of chronic asthma.

Beyond improvements in inhaled bronchodilators and corticosteroids to enhance their efficacy, duration of action and safety, the discovery of new anti-asthma drugs has largely been driven by animal models of allergen sensitization and challenge.

Recent studies have demonstrated an anti-inflammatory action of muscarinic antagonists which includes abrogation of animal models of allergen challenge 4, reduction in neutrophil elastase activity 37 and modification of growth factors, such as EGF and TGFβ 38, 39.

Systematic progress has been made from in vitro human models of allergen T cell epitope-based peptide anergy in the early 1990s, through proof-of-concept murine allergy models and early human trials with longer peptides, to the current randomized, double-blind, placebo-controlled clinical trials with the potential new class of synthetic short immune-regulatory T cell epitope peptide therapies.

In contrast, anti−IL-9 antibody therapy has led to reduced levels of AHR in murine models of allergen-induced asthma [ 13, 14].

In murine models of allergen-dependent asthma, the proinflammatory cytokine TNF- α, produced by Th1 lymphocytes, macrophages and mast cells, induced airway recruitment of neutrophils and eosinophils via upregulation of epithelial and endothelial adhesion molecules [ 38].

In murine models of allergen-induced asthma, blockade of either IL-4 or its receptor has been shown to inhibit eosinophil influx into the airways and IL-5 release from T cells, as well as decreasing lung inflammation, serum IgE levels, and airway hyperresponsiveness to methacholine [ 70, 71].

Epitope sequences were obtained from previously published literature and manually mapped onto spacefill models of allergens using CLUSTALX v1.83 [ 85] to align sequences, Genedoc v2.6.002 [ 86] to visualise the resulting pileups and Rasmol v2.7.2.1.1 [ 87] to colour structures.

In the current study, pharmacological activity of inhibition of the OX40L OX40 pathway was evaluated in subjects with mild allergic asthma using a model of allergen inhalation challenge.

To explore the role of IL-28 cytokines in allergic airway disease, we used an established mouse model of allergen sensitization and challenge (Fig 1A).

administration, Cpd #15, at 0.1 μmol/kg significantly inhibited and at 1 μmol/kg fully counteracted eosinophilic infiltration in a model of allergen-induced pulmonary inflammation in rats.