Vascular remodeling is a feature of asthma and nonasthmatic eosinophilic bronchitis

Siddiqui, Salman; Sutcliffe, Amanda; Shikotra, Aarti; Woodman, Lucy; Doe, Camille; McKenna, Susan; Wardlaw, Andrew J.; Bradding, Peter; Pavord, Ian D.; Brightling, Christopher E.

doi:10.1016/j.jaci.2007.05.028

Cited by 86 publications

(81 citation statements)

References 40 publications

(41 reference statements)

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“…However, the duration of disease in the nonasthmatic eosinophilic bronchitis cohort in the study by KANAZAWA et al [112] is unclear and disease duration is critical in assessing the impact of some features of airway remodelling [113]. The current authors have recently demonstrated in patients with chronic nonasthmatic eosinophilic bronchitis that vascular remodelling does occur to a similar degree as in moderate-tosevere persistent asthma and is, therefore, unlikely to be related to AHR [114]. The increased vascularity in asthma was related to disease duration and airflow obstruction, but not AHR.…”

Section: Inflammatory Cell Localisation To Vasculaturementioning

confidence: 97%

Inflammatory cell microlocalisation and airway dysfunction: cause and effect?

Siddiqui

Hollins²,

Saha³

et al. 2007

European Respiratory Journal

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Airway inflammation is a critical feature of the airway diseases asthma and chronic obstructive pulmonary disease (COPD). There is emerging evidence that structural cells play a key role in the development and perpetuation of the inflammatory response and are pivotal in the development of the changes in the airway structures that lead to airway remodelling.To date, little attention has been given to the localisation of inflammatory cells to airway structures or the potential interactions between these intimately located cells. However, it is likely that interactions between inflammatory and structural cells in the airway contribute enormously to the pathophysiology of asthma and COPD.Indeed, recent evidence suggests that mast cells localised to the airway smooth muscle bundle may be important in the development of airway hyperresponsiveness in asthma.In the present article, the authors aim to summarise: 1) the current understanding of which inflammatory cells locate to airway structures; 2) the proposed mechanisms that may be involved in mediating this microlocalisation; 3) the possible consequences of interactions between inflammatory and structural cells; and 4) the pressing need to investigate whether modulating these interactions is beneficial in asthma and chronic obstructive pulmonary disease.

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Section: Inflammatory Cell Localisation To Vasculaturementioning

confidence: 97%

Inflammatory cell microlocalisation and airway dysfunction: cause and effect?

Siddiqui

Hollins²,

Saha³

et al. 2007

European Respiratory Journal

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“…VEGF plays an important role in regulating the growth of new vessels and vascular leakage in asthmatic airways (83). Increased expression of VEGF and VEGF receptors is correlated with increased vascularity in asthmatic airways (84).…”

Section: Egf Egf Activates Egfr Tyrosine Kinases That Are Also Acti-mentioning

confidence: 99%

The cytokine network in asthma and chronic obstructive pulmonary disease

Barnes¹

2008

J. Clin. Invest.

821

714

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Asthma and chronic obstructive pulmonary disease (COPD) are very common inflammatory diseases of the airways. They both cause airway narrowing and are increasing in incidence throughout the world, imposing enormous burdens on health care. Cytokines play a key role in orchestrating the chronic inflammation and structural changes of the respiratory tract in both asthma and COPD and have become important targets for the development of new therapeutic strategies in these diseases. IntroductionThe most common inflammatory diseases of the airways are asthma and chronic obstructive pulmonary disease (COPD), and the incidence of both is increasing throughout the world. The prevalence of asthma in developed countries is approximately 10% in adults and even higher in children, whereas in developing countries, the prevalence is lower but increasing rapidly. The global prevalence of COPD is approximately 10% among individuals over the age of 40 years. Asthma often starts in early childhood and is characterized by intermittent wheezing and shortness of breath. In contrast, the predominant symptom in COPD is shortness of breath on exertion, which is persistent and slowly progressive. Although the clinical symptoms of both diseases are caused by airway narrowing as a result of inflammation in the airways, there are marked differences in the patterns of underlying inflammation.Cytokines play a key role in orchestrating the chronic inflammation of asthma and COPD by recruiting, activating, and promoting the survival of multiple inflammatory cells in the respiratory tract (Figure 1, Figure 2, and Table 1). Over 50 cytokines have now been identified in asthma and COPD, but their role in the pathophysiology of these complex airway diseases is often unclear. For the purpose of this Review, cytokines are classified into lymphokines (cytokines that are secreted by T cells and regulate immune responses), proinflammatory cytokines (cytokines that amplify and perpetuate the inflammatory process), growth factors (cytokines that promote cell survival and result in structural changes in the airways), chemokines (cytokines that are chemotactic for inflammatory cells), and antiinflammatory cytokines (cytokines that negatively modulate the inflammatory response), although many of these functions may overlap. Where possible, I have focused on human studies and have emphasized any therapeutic interventions that have been made.

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“…Kanazawa et al [29] reported that the production of VEGF and airway permeability were increased in asthmatics but not in patients with EBWA. However, Siddiqui et al [30] found a similar increase in sputum VEGF concentrations in both subgroups.…”

Section: Etiology and Pathogenesismentioning

confidence: 88%

Eosinophilic Bronchitis without Asthma

Gönlügür

Gönlügür²

2008

Int Arch Allergy Immunol

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Background: Eosinophilic bronchitis without asthma causes chronic coughs without the physiologic features of asthma. The aim of this study was to review the clinical features, pathogenesis, diagnosis, treatment and prognosis of this condition. Methods: The current literature was reviewed using Pubmed for all studies published in the English language using the search term ‘eosinophilic bronchitis’. Results: Eosinophilic bronchitis presents as normal spirometry, without evidence of airway hyperresponsiveness, and normal peak expiratory flow variability. When compared with asthma, mast cell recruitment to the superficial airways and mast cell activation appear to be a feature of eosinophilic bronchitis. In contrast, mast cell infiltration in the smooth muscle is significantly higher in asthma patients than in either eosinophilic bronchitis patients or healthy control subjects. In this condition, the absence of high IL-13 expression can contribute to the normal airway reactivity. The cough usually responds well to inhaled corticosteroids but dose and duration of treatment remain unclear. The condition can be transient, episodic or persistent unless treated, and occasionally, patients may require long-term treatment with oral corticosteroids. Conclusions: The condition is an important cause of chronic coughs which are corticosteroid responsive. The study of eosinophilic bronchitis suggests that eosinophil-dependent mechanisms are generally not important in the pathogenesis of asthma.

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Vascular remodeling is a feature of asthma and nonasthmatic eosinophilic bronchitis

Cited by 86 publications

References 40 publications

Inflammatory cell microlocalisation and airway dysfunction: cause and effect?

Inflammatory cell microlocalisation and airway dysfunction: cause and effect?

The cytokine network in asthma and chronic obstructive pulmonary disease

Eosinophilic Bronchitis without Asthma

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