Increased immunoreactivity of stromal cell-derived factor‐1 and angiogenesis in asthma

Hoshino, Makoto; Aoike, Nozomi; Takahashi, Miki; Nakamura, Yutaka; Nakagawa, Takemasa

doi:10.1183/09031936.03.00082002

Cited by 42 publications

(33 citation statements)

References 27 publications

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“…Furthermore, in lung-targeted transgenic mice, selective overexpression of VEGF induced an asthma-like phenotype with vascular remodelling (angiogenesis, hyperpermeability, oedema formation) [143] and extravascular remodelling (mucus metaplasia, myocyte hyperplasia, airway hyperresponsiveness) in the airways [144]. In addition, tumour necrosis factor-a, transforming growth factor-a, interleukin-8 [145], matrix remodelling proteases [146], stromal cell-derived factor-1 [140], basic fibroblast growth factor [147], and angiogenin [16] have all been proposed to have some role in angiogenesis and microvascular remodelling in asthma.…”

Section: Angiogenesis and Microvascular Remodellingmentioning

confidence: 99%

Inhaled corticosteroids: effects on the airway vasculature in bronchial asthma

Horváth

Wanner²

2006

European Respiratory Journal

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Inhaled corticosteroids suppress airway inflammation and components of airway remodelling in bronchial asthma. In the tracheobronchial (airway) vasculature, these include the inhibition of inflammatory hyperperfusion, microvascular hyperpermeability, mucosal oedema formation, and the formation of new blood vessels (angiogenesis).Corticosteroids are now known to exert their effects on the airway vasculature through genomic and nongenomic mechanisms. Genomic actions involve the regulation of target genes, and suppress most of the vascular elements of inflammation and angiogenesis in the airway. In contrast, nongenomic actions are mediated by rapid cellular mechanisms, and induce transient vasoconstriction in the airway, thereby reversing inflammatory hyperperfusion.The vascular actions of corticosteroids contribute to controlling clinical symptoms of asthma primarily by influencing airway calibre in the lung periphery and airway hyperreactivity.In this review article, recent advances into the understanding of cellular mechanisms and the clinical implications of the interaction of inhaled corticosteroids and the airway vasculature in asthma are reviewed.

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Section: Angiogenesis and Microvascular Remodellingmentioning

confidence: 99%

Inhaled corticosteroids: effects on the airway vasculature in bronchial asthma

Horváth

Wanner²

2006

European Respiratory Journal

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“…Another report on allergic mice demonstrated that treatment with CXCR4 antagonist AMD3100 reduced airway hyperreactivity, peribronchial eosinophilia, and inflammatory responses [101]. Hoshino et al reported an increased immunoreactivity of CXCL12 in bronchial biopsies of subjects with asthma and suggested that positive cells could play a role in airway remodeling via angiogenesis [102]. In human asthma, there is a report that establishes a direct relationship between CXCL12 expression and cellular mobilization into the airways (Negrete-Garcia, MC, et al Chest in press).…”

Section: Cxcr4mentioning

confidence: 99%

Chemokines and Their Receptors in the Allergic Airway Inflammatory Process

Velázquez

Teran

2010

Clinic Rev Allerg Immunol

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The development of the allergic airway disease conveys several cell types, such as T-cells, eosinophils, mast cells, and dendritic cells, which act in a special and temporal synchronization. Cellular mobilization and its complex interactions are coordinated by a broad range of bioactive mediators known as chemokines. These molecules are an increasing family of small proteins with common structural motifs and play an important role in the recruitment and cell activation of both leukocytes and resident cells at the allergic inflammatory site via their receptors. Trafficking and recruitment of cell populations with specific chemokines receptors assure the presence of reactive allergen-specific T-cells in the lung, and therefore the establishment of an allergic inflammatory process. Different approaches directed against chemokines receptors have been developed during the last decades with promising therapeutic results in the treatment of asthma. In this review we explore the role of the chemokines and chemokine receptors in allergy and asthma and discuss their potential as targets for therapy.

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“…Cultured human and murine fibrocytes express the receptor for CXCL12 (also known as stromal cell-derived factor-1) [35], a cytokine produced by bronchial epithelial cells and potentially involved in the promotion of airway inflammation in asthma [70,71]. CXCL12 induces a migratory response in bone marrow-derived progenitors and inflammatory cells by aptotaxis, after binding to ECM components such as fibronectin and proteoglycans [72][73][74][75].…”

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confidence: 99%

Interactions between the Bronchial Epithelium and Fibrocytes in the Pathogenesis of Airway Remodeling in Asthma

Bellini¹

2013

JEBP

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Abstract:The histopathologic features of asthma include chronic airway inflammation, increased density of fibroblasts and myofibroblasts in the lamina propria and presence of structural abnormalities of the bronchial wall collectively referred to with the term "airway remodeling". The newly emerged population of fibroblasts and myofibroblasts contributes to airway remodeling by producing excessive amounts of collagenous and non-collagenous extracellular matrix components in the subepithelial zone and by expanding the mass of contractile cells in the bronchial wall. A substantial proportion of these mesenchymal cells in asthma exhibit the phenotypic and functional characteristic of fibrocytes, which represent a unique population of bone marrow-derived mesenchymal progenitors recruited to tissue sites from the circulation in response to injury or in chronic inflammatory conditions. Recent studies have demonstrated that the asthmatic bronchial epithelium is a major source of fibrocyte chemoattractants and growth factors. This review will focus on the novel observations suggesting that asthmatic epithelial cells may play a key role in the development and progression of airway remodeling by promoting the recruitment and local differentiation of fibrocytes.

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Increased immunoreactivity of stromal cell-derived factor‐1 and angiogenesis in asthma

Cited by 42 publications

References 27 publications

Inhaled corticosteroids: effects on the airway vasculature in bronchial asthma

Inhaled corticosteroids: effects on the airway vasculature in bronchial asthma

Chemokines and Their Receptors in the Allergic Airway Inflammatory Process

Interactions between the Bronchial Epithelium and Fibrocytes in the Pathogenesis of Airway Remodeling in Asthma

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