Original articleCharacterization of allergen-induced bronchial hyperresponsiveness and airway inflammation in actively sensitized Brown-Norway rats☆
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Bronchoprovocation Testing in Asthma: An Update
2018, Immunology and Allergy Clinics of North AmericaAnti-asthmatic effects of type-A procyanidine polyphenols from cinnamon bark in ovalbumin-induced airway hyperresponsiveness in laboratory animals
2013, Biomedicine and Aging PathologyCitation Excerpt :The role of antigen stimuli recruitment and eosinophils activation during AHR is well-established [8,34]. Inflammatory mediators play a key role in the pathogenesis of AHR by producing bronchoactive mediators, which participate in the development of airway inflammation [8,35]. Eosinophil is one of the primary effector cells responsible for the induction of the allergen inflammation.
Bronchoprovocation Testing in Asthma
2012, Immunology and Allergy Clinics of North AmericaCitation Excerpt :Evidence in support of this relationship can be grouped according to associations between inflammatory and allergic markers and BHR, and modification of BHR and inflammatory markers using anti-inflammatory medications. Sensitization and allergen challenge or exposure in animal and human studies using single or repeated doses induces airway reactivity that is associated with a variety of immunologic features, such as production of antigen specific IgE levels, up-regulation of T-helper cytokines, early and late-phase reactions, and eosinophilic inflammation.34–37 After allergen stimulation, the influx of inflammatory cells in the airways, notably eosinophils, precedes the development of late-phase response, and correlates with an increase in BHR.
Effect of mometasone furoate (MF)/formoterol fumarate (F) combination (MF/F) on late-phase responses in allergen-challenged Brown Norway rats
2011, Pulmonary Pharmacology and TherapeuticsCitation Excerpt :The combination index of MF/F for inhibition inflammatory cells, cytokines and improvement in lung function was generally <1 suggesting that drug synergy exists for the MF/F combination. The allergen-challenged Brown Norway rat displays many of the important features of human asthma such as acute and late-phase airflow obstruction [9,18,19], bronchial hyper-responsiveness [20,21], inflammatory cell influx into the lungs [8,9,19–21], production of pro-inflammatory mediators and cytokines [19,21] and mucus hypersecretion [9]. In this study, evaluations were performed on the late-phase reduction in lung function, measured by the decrease in FVC, the numbers of inflammatory cells, including eosinophils and neutrophils, and levels of pro-inflammatory cytokines, including IL-4, IL-5, IL-13 and TNF-α in the BAL fluid of sensitized rats following aerosolized ovalbumin challenge.
Kidins220/ARMS contributes to airway inflammation and hyper-responsiveness in OVA-sensitized mice
2011, Respiratory Physiology and NeurobiologyCitation Excerpt :All groups contained 12 mice except the OVA group, which had 16 mice. Sensitization and challenge protocols were carried out according to the methods of Elwood et al. (1991) and Vanacker et al. (2001) with some modifications (as described below). On days 0, 7, 14 and 21, all mice except the control group were actively sensitized with OVA (1 mg, i.p.; Sigma–Aldrich, St Louis, MO, USA) and 100 mg aluminum hydroxide in 0.5 mL phosphate-buffered saline (PBS).
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Supported by the National Asthma Campaign (U.K.), and Medical Research Council (U.K.).