Quantitative Analysis of Bronchial Wall Vascularity in the Medium and Small Airways of Patients With Asthma and COPD

Hashimoto, Midori; Tanaka, Hiroshi; Abe, Shosaku

doi:10.1378/chest.127.3.965

Cited by 142 publications

(141 citation statements)

References 24 publications

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“…As previously underlined by several authors, there is a remarkable proliferative capacity of the bronchial vessels in response to a variety of pulmonary diseases [18,19]. In a recent study, HASHIMOTO et al [20] reported that submucosal vascularity in patients with COPD was greater than in control subjects, but not significantly, except for the proportion of vascularity in the small airways. These data are consistent with the results of previous studies [21].…”

Section: Discussionmentioning

confidence: 86%

Cryptogenic haemoptysis in smokers: angiography and results of embolisation in 35 patients

Menchini¹,

Rémy‐Jardin²,

Faivre³

et al. 2009

Eur Respir J

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The aim of the present study was to describe angiographic findings and embolisation results in smokers with haemoptysis.We retrospectively reviewed the clinical data and angiographic findings from 35 patients with smoking-related bronchopulmonary disease and no associated comorbidity, who were referred for embolisation for mild (n56), moderate (n514) and severe (n515) haemoptysis. Spirometric classification subdivided our population into: 16 patients with chronic bronchitis but no airflow limitation; and 19 patients with chronic obstructive pulmonary disease (COPD) (stage I: n512; stage II: n55; stage III: n52).Bronchoscopy depicted focal submucosal vascular abnormalities in three patients and only endobronchial inflammation in 32 (91%) patients. Bronchial artery angiography revealed moderate (n518) or severe (n510) hypervascularisation in 28 (80%) patients, and normal vascularisation in seven (20%). No statistically significant difference was observed between the angiographic findings and the severity of COPD, tobacco consumption or the amount of bleeding. Cessation of bleeding was obtained by embolisation in 29 out of the 34 technically successful procedures (85%), requiring surgery in three out of five patients with recurrence. Follow-up (mean duration 7 yrs) demonstrated no recurrence of bleeding in 32 (94%) out of 34 patients and excluded late endobronchial malignancy.Smokers with various stages of COPD severity may suffer from haemoptysis that is efficiently treatable by endovascular treatment.

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Section: Discussionmentioning

confidence: 86%

Cryptogenic haemoptysis in smokers: angiography and results of embolisation in 35 patients

Menchini¹,

Rémy‐Jardin²,

Faivre³

et al. 2009

Eur Respir J

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“…This may reflect their role in adhesion, extravasation, and possibly activation of inflammatory cells, especially eosinophils. Furthermore, it might contribute to angiogenesis, which is thought to play a role in asthma and COPD as well [47,48]. Furthermore, angiogenesis is important in tumor development; EGFRsignaling of ADAMs may contribute in this way [3].…”

Section: Discussionmentioning

confidence: 99%

Expression of ADAMs (“a disintegrin and metalloprotease”) in the human lung

et al. 2009

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In view of the associations of "a disintegrin and metalloprotease" (ADAM) with respiratory diseases, we assessed the expression of various ADAMs in human lung tissue. Lung tissue was obtained from nine individuals who underwent surgery for lung cancer or underwent lung transplantation for emphysema. Also, 16HBE 14o-(human bronchial epithelial) and A549 (alveolar type II epitheliumlike) cell lines were used. Immunohistochemistry was performed with antibodies recognizing different ADAM domains. The ADAMs were typically distributed over the bronchial epithelium. ADAM8 and ADAM10 were expressed diffusely in all layers of the epithelium. ADAM9, ADAM17, and ADAM19 were predominantly expressed in the apical part of the epithelium, and ADAM33 was predominantly and strongly expressed in basal epithelial cells. In smooth muscle, ADAM19 and ADAM17 were strongly expressed, as was ADAM33, though this expression was weaker. ADAM33 was strongly expressed in vascular endothelium. All ADAMs were generally expressed in inflammatory cells. The typical distribution of ADAMs in the lung, especially in the epithelium, is interesting and suggests a localized function. As most ADAMs are involved in release of (pro-) inflammatory mediators and growth factors, they may play an important role in the first line of defense and in initiation of repair events in the airways.

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“…Vascular remodelling occurs in asthma and COPD [108][109][110][111] and is associated with airflow obstruction [108]. The role of vascular remodelling in the development of AHR in asthma is contentious.…”

Section: Inflammatory Cell Localisation To Vasculaturementioning

confidence: 99%

Inflammatory cell microlocalisation and airway dysfunction: cause and effect?

Siddiqui

Hollins²,

Saha³

et al. 2007

Eur Respir J

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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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Quantitative Analysis of Bronchial Wall Vascularity in the Medium and Small Airways of Patients With Asthma and COPD

Cited by 142 publications

References 24 publications

Cryptogenic haemoptysis in smokers: angiography and results of embolisation in 35 patients

Cryptogenic haemoptysis in smokers: angiography and results of embolisation in 35 patients

Expression of ADAMs (“a disintegrin and metalloprotease”) in the human lung

Inflammatory cell microlocalisation and airway dysfunction: cause and effect?

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