Increased vascular permeability precedes cellular inflammation as asthma control deteriorates

Khor, YH; Teoh, A. K. Y.; Lam, SK; Mo, Doss; Weston, S; Reid, David W.; Walters, E. Haydn

doi:10.1111/j.1365-2222.2009.03349.x

Cited by 51 publications

(58 citation statements)

References 54 publications

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“…Oedema would act to thicken the airway wall, therefore decreasing lumen size. Increased vascular permeability occurs as asthma control deteriorates [75]; however, oedema is not related to changes in AHR during allergen challenges [76]. This finding is supported by studies in animals that have found that oedema causes only modest airway narrowing [77].…”

Section: Do Respiratory Viral Infections Reduce B 2 -Agonist Efficacy?supporting

confidence: 74%

Viral infections and asthma: an inflammatory interface?

et al. 2014

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Asthma is a chronic inflammatory disease of the airways in which the majority of patients respond to treatment with corticosteroids and b 2 -adrenoceptor agonists. Acute exacerbations of asthma substantially contribute to disease morbidity, mortality and healthcare costs, and are not restricted to patients who are not compliant with their treatment regimens. Given that respiratory viral infections are the principal cause of asthma exacerbations, this review article will explore the relationship between viral infections and asthma, and will put forward hypotheses as to why virus-induced exacerbations occur. Potential mechanisms that may explain why current therapeutics do not fully inhibit virus-induced exacerbations, for example, b 2 -adrenergic desensitisation and corticosteroid insensitivity, are explored, as well as which aspects of virus-induced inflammation are likely to be attenuated by current therapy. @ERSpublications Why do virus-induced asthma exacerbations occur? Mechanisms and interventions

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Section: Do Respiratory Viral Infections Reduce B 2 -Agonist Efficacy?supporting

confidence: 74%

Viral infections and asthma: an inflammatory interface?

et al. 2014

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“…Markers of vascular permeability; perivascular albumin staining and BALf microalbumin levels were also elevated in these asthmatic subjects on high-dose inhaled corticosteroid therapy compared to healthy controls and airway albumin levels correlated with infiltrating T lymphocytes. The proportion of airway vascularity (number and size of blood vessels) and VEGF levels in this cohort of asthmatic subjects was not altered when the dose of fluticasone propionate was halved and associated with clinical asthma deterioration yet without the return of cellular inflammation [81] suggesting that vascular leakage is a feature of asthma deterioration that may precede the return of cellular inflammation.…”

Section: Vascular Inflammation and Remodelling Processes In Asthmamentioning

confidence: 73%

Pulmonary vascular changes in asthma and COPD

Harkness

Kanabar

Sharma

et al. 2014

Pulmonary Pharmacology & Therapeutics

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In chronic lung disorders such as in asthma and chronic obstructive pulmonary disease (COPD) there is increased bronchial angiogenesis and remodelling of pulmonary vessels culminating to altered bronchial and pulmonary circulation. The involvement of residential cells such as endothelial cells, smooth muscle cells and pulmonary fibroblasts, all appear to have a crucial role in the progression of vascular inflammation and remodelling. The regulatory abnormalities, growth factors and mediators implicated in the pulmonary vascular changes of asthma and COPD subjects and potential therapeutic targets have been described in this review.

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“…We demonstrated that Nrf2 reduces airway leakiness in vivo. Both in vitro and in vivo studies have shown that the airway epithelium of individuals with asthma is leakier than in normal subjects (21,59). To further address the role of Nrf2 in barrier function, we performed ex vivo experiments using tracheal epithelial cells from Tam-Keap1 Ϫ/Ϫ and CC10-Keap1…”

Section: Discussionmentioning

confidence: 99%