Ultrastructure of bronchial biopsies from patients with allergic and non-allergic asthma

Shahana, Shahida; Björnsson, E.; Lúdvı́ksdóttir, Dóra; Janson, Christer; Nettelbladt, O; Venge, Per; Roomans, Godfried M.

doi:10.1016/j.rmed.2004.08.013

Cited by 59 publications

(55 citation statements)

References 41 publications

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“…In most forms of asthma, the bronchial mucosa of patients shows structural and functional abnormalities of the bronchial epithelium, an inflammatory infiltrate mainly composed of activated T lymphocytes, CD14 þ monocytes, eosinophils and mast cells, and remodeling of the airway tissue architecture. [60][61][62][63][64][65][66] Peculiar aspects of the remodeling process include angiogenesis, the accumulation of fibroblasts and myofibroblasts below the epithelial basement membrane, thickening of the lamina reticularis as a result of an excessive deposition of ECM molecules and bronchial smooth muscle cells hyperplasia. [65][66][67][68][69][70] Repeated cycles of airway inflammation and repair with unsuccessful healing are thought to represent the driving force for most of these structural alterations, 66 as the bronchial mucosa of asthmatic patients resembles a wounded tissue where neither the inflammatory phase nor the reparative phase resolves completely.…”

Section: Airway Remodeling In Asthmamentioning

confidence: 99%

The role of the fibrocyte, a bone marrow-derived mesenchymal progenitor, in reactive and reparative fibroses

Bellini¹,

Mattoli²

2007

Laboratory Investigation

384

403

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Human fibrocytes are mesenchymal progenitors that exhibit mixed morphological and molecular characteristics of hematopoietic stem cells, monocytes and fibroblasts. They likely represent the obligate intermediate stage of differentiation into mature mesenchymal cells of a bone marrow-derived precursor of the monocyte lineage under permissive conditions. On in vitro stimulation with pro-fibrotic cytokines and growth factors, human fibrocytes produce large quantities of extracellular matrix components and further differentiate into cells identical to the contractile myofibroblasts that emerge at the tissue sites during repair processes and in some fibrotic lesions. Studies in various animal models of wound healing or fibrotic diseases have confirmed the ability of fibrocytes to differentiate into mature mesenchymal cells in vivo and have suggested a causal link between fibrocyte accumulation and ongoing tissue fibrogenesis or vascular remodeling in response to tissue damage or hypoxia. Fibrocytes synthesizing new collagen or acquiring myofibroblast markers have been detected in human hypertrophic scars, in the skin of patients affected by nephrogenic systemic fibrosis, in human atherosclerotic lesions, and in pulmonary diseases characterized by repeated cycles of inflammation and repair, like asthma. The presence of fibrocyte-like cells has been reported in human chronic pancreatitis and chronic cystitis. Similar cells also populate the stroma surrounding human benign tumors. The available data indicate that human fibrocytes serve as a source of mature mesenchymal cells during reparative processes and in fibrotic disorders or stromal reactions predominantly associated with a persistent inflammatory infiltrate or with the selective recruitment of monocytes induced by ischemic changes and tumor development. A deeper understanding of the mechanisms involved in fibrocyte differentiation in these pathological conditions may lead to the development of novel therapies for preventing detrimental tissue or vascular remodeling and metastatic progression of invasive tumors.

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Section: Airway Remodeling In Asthmamentioning

confidence: 99%

The role of the fibrocyte, a bone marrow-derived mesenchymal progenitor, in reactive and reparative fibroses

Bellini¹,

Mattoli²

2007

Laboratory Investigation

384

403

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“…However, this study was based on morphometry and did not use markers of epithelial repair to discriminate between damage that had occurred in vivo and artefactual damage that inevitably arises due to the bronchoscopy procedure [12]. More recent ultrastructural studies have provided further insight into the structure of the asthmatic epithelium, where it has been suggested that reduced desmosomal contact may be an important factor in the epithelial shedding observed in patients with asthma [13]. In vitro studies have also identified functional differences in the responses of asthmatic epithelial cells to environmental injury.…”

Section: Airway Remodelling In Asthma Epithelial Changesmentioning

confidence: 99%

The contribution of transforming growth factor- and epidermal growth factor signalling to airway remodelling in chronic asthma

Boxall

Holgate²,

Davies³

2006

European Respiratory Journal

222

187

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Asthma is increasing in prevalence in the developing world, affecting ,10% of the world's population. It is characterised by chronic lung inflammation and airway remodelling associated with wheezing, shortness of breath, acute bronchial hyperresponsiveness to a variety of innocuous stimuli and a more rapid decline in lung function over time.Airway remodelling, involving proliferation and differentiation of mesenchymal cells, particularly myofibroblasts and smooth muscle cells, is generally refractory to corticosteroids and makes a major contribution to disease chronicity. Transforming growth factor-b is a potent profibrogenic factor whose expression is increased in the asthmatic airways and is a prime candidate for the initiation and persistence of airway remodelling in asthma.This review highlights the role of transforming growth factor-b in the asthmatic lung, incorporating biosynthesis, signalling pathways and functional outcome. In vivo, however, it is the balance between transforming growth factor-b and other growth factors, such as epidermal growth factor, which will determine the extent of fibrosis in the airways.A fuller comprehension of the actions of transforming growth factor-b, and its interaction with other signalling pathways, such as the epidermal growth factor receptor signalling cascade, may enable development of therapies that control airway remodelling where there is an unmet clinical need.

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“…This is likely to be important, as it places these cells at the mucosal interface with pathogenic and allergic stimuli promoting an effector role for inflammatory cells in the ongoing immune response and facilitating cellular interactions. In asthma and healthy subjects, T-cells are the most abundant inflammatory cell in the epithelium [20,25,27,28] but increased numbers of T-cells in the epithelium in disease is rarely reported [20], and most studies do not support the view that T-cells are selectively recruited to the epithelium [21,27]. Similarly, in COPD, both granulocytes and T-cell numbers have been shown to be increased in the epithelium in some studies [31,35] but not in all [31,33,34].…”

Section: Inflammatory Cell Localisation To Mucus Glandsmentioning

confidence: 99%

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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Ultrastructure of bronchial biopsies from patients with allergic and non-allergic asthma

Cited by 59 publications

References 41 publications

The role of the fibrocyte, a bone marrow-derived mesenchymal progenitor, in reactive and reparative fibroses

The role of the fibrocyte, a bone marrow-derived mesenchymal progenitor, in reactive and reparative fibroses

The contribution of transforming growth factor- and epidermal growth factor signalling to airway remodelling in chronic asthma

Inflammatory cell microlocalisation and airway dysfunction: cause and effect?

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