Asthma: a disease remodeling the airways

Bousquet, Jean; Chanez, Pascal; Lacoste, J.-Y.; White, R. J.; Vic, P.; Godard, P.; Michel, F.B.

doi:10.1111/j.1398-9995.1992.tb02242.x

Cited by 243 publications

(162 citation statements)

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“…Asthma is a chronic inflammatory disease associated with remodelling of the airways [2], including subepithelial fibrosis [3]. Chronic bronchitis is another chronic obstructive disease of the airways in which inflammation is followed by fibrosis with extracellular matrix (ECM) deposition on the airways wall [4].…”

Section: Introductionmentioning

confidence: 99%

Release of transforming growth factor-beta (TGF-β) and fibronectin by alveolar macrophages in airway diseases

Vignola¹,

Chanez

Chiappara³

et al. 1996

Clinical and Experimental Immunology

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SUMMARYAsthma and chronic bronchitis are associated with airway remodelling, and airway macrophages are present in bronchial inflammation. TGF-¯and fibronectin released by alveolar macrophages possess a fibrogenic potency. The potential role of alveolar macrophages in airway remodelling was studied in asthma and chronic bronchitis by the release of TGF-¯and fibronectin. Alveolar macrophages were isolated by bronchoalveolar lavage in 14 control subjects, 14 asthmatics and 14 chronic bronchitics. The spontaneous and lipopolysaccharide (LPS)-or concanavalin A (Con A)-induced release of TGF-¯and fibronectin was measured by ELISA. Alveolar macrophages from chronic bronchitics spontaneously release greater amounts of TGF-¯and fibronectin than those from asthmatic and control subjects. Alveolar macrophages from asthmatics release greater amounts of TGF-¯and fibronectin than those from control subjects. The spontaneous release of TGF-¯is significantly correlated with that of fibronectin. Fibronectin release was significantly reduced after LPS stimulation, and TGF-¯release was significantly increased after LPS stimulation, except in chronic bronchitis patients. Con A increased the release of TGF-¯in cells from normal subjects. This study suggests that activated macrophages play a role in airway remodelling in chronic bronchitis and to a lesser extent in asthma.

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Section: Introductionmentioning

confidence: 99%

Release of transforming growth factor-beta (TGF-β) and fibronectin by alveolar macrophages in airway diseases

Vignola¹,

Chanez

Chiappara³

et al. 1996

Clinical and Experimental Immunology

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“…This latter probably leads to an increased rate of lung function decrease during the life (Lange et al, 1998). The main structural changes described in bronchi of asthmatics are: (a) an epithelial thickening and a sub-epithelial fibrosis mainly linked to deposition of different collagen subtypes (types I and III) and fibronectin, (b) some changes of extracellular matrix composition (e.g., elastic fibres fragmentation, tenascin deposition,...), (c) smooth muscle cell hyperplasia, (d) mucus-producing cells ("Goblet cells") hyperplasia, (e) increase in the surface of blood vessels in airway walls, and (f) perichondral fibrosis (Bousquet et al, 1992;Cataldo et al, 2003;Vignola et al, 1998a).…”

Section: Implication Of Mmps In the Pathogenesis Of Asthmamentioning

confidence: 99%

Section: Implication Of Mmps In the Pathogenesis Of Asthmamentioning

confidence: 99%

“…533, iss.1-3, pp. 133-144 Status: Postprint (Author's version) tenascin deposition,...), (c) smooth muscle cell hyperplasia, (d) mucus-producing cells ("Goblet cells") hyperplasia, (e) increase in the surface of blood vessels in airway walls, and (f) perichondral fibrosis (Bousquet et al, 1992;Cataldo et al, 2003;Vignola et al, 1998a).MMP-9 was the first MMP to be studied in depth for its implication in pathology of asthma. Increased levels of MMP-9 were indeed detected in bronchoalveolar lavage fluid (Mautino et al, 1997), sputum induced by the inhalation of hypertonic saline (Cataldo et al, 2000;Vignola et al, 1998b) and in serum of asthmatic patients (Bosse et al, 1999).…”

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confidence: 99%

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Matrix metalloproteinases (MMPs) and tissue inhibitors of MMPs in the respiratory tract: Potential implications in asthma and other lung diseases

Guéders

Foidart

Noël

et al. 2006

European Journal of Pharmacology

279

224

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In healthy lung, Matrix Metalloproteinases (MMPs) and their physiological inhibitors, tissue inhibitors of matrix metalloproteinases (TIMPs), are produced in the respiratory tract by a panel of different structural cells. These activities are mandatory for many physiological processes including development, wound healing and cell trafficking. Deregulation of proteolytic-antiproteolytic network and inappropriate secretion of various MMPs by stimulated structural or inflammatory cells is thought to take part to pathophysiology of numerous lung diseases including asthma, chronic obstructive pulmonary disease (COPD), lung fibrosis and lung cancer. Cytokines and growth factors are involved in these inflammatory processes and some of those mediators interact directly with MMPs and TIMPs leading either to a regulation of their expression or changes in their biological activities by proteolytic cleavage. In turn, cytokines and growth factors modulate secretion of MMPs establishing a complex network of reciprocal interactions. Every MMP seem to play a rather specific role and some variations of their expression are observed in different lung diseases. The precise role of these enzymes and their inhibitors is now studied in depth as they could represent relevant therapeutic targets for many diseases. Indeed, MMP inhibition can lead either to a decrease of the intensity of a pathological process or, in the contrary for some of them, to an increase of disease severity. In this review, we focus on the role played by MMPs and TIMPs in asthma and we provide an overview of their potential roles in COPD, lung fibrosis and lung cancer, with a special emphasis on loops including MMPs and cytokines and growth factors relevant in these diseases.Keywords: Matrix metalloproteinase; Tissue inhibitor of MMP; Asthma; Cytokine; Growth factors Matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs)Matrix metalloproteinases (MMPs), or matrixins, belong to the metzincin superfamily of metalloproteinases, also including astacins, ADAMs (a protein with a disintegrin and metallopro-tease domain) and ADAM-TS proteases (ADAM with a thrombospondin-like motif) (Sternlicht and Werb, 2001;Folgueras et al., 2004;Handsley and Edwards, 2005;Noel et al., 2004). MMPs are proteolytic enzymes believed to be implicated in many physiological and pathological processes including embryonic development, morphogenesis, reproductive processes, bone remodeling, wound healing, cancer, arthritis, atherosclerosis, MMPs are zinc and calciumdependent enzymes being able to degrade virtually all extracellular matrix components. This can modulate cell behaviour by creating influential cellular environment (Shapiro, 1998). The extracellular matrix is a complex network of molecules including collagens, fibronectin, laminin, entactin/ nidogen and heparan sulfate proteoglycans (Mott and Werb, 2004). The extracellular matrix is a mechanical support for cells but also acts as a reservoir for cytokines and growth factors (vascular endothelial ...

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“…We also show that human circulating fibrocytes acquire the myofibroblast phenotype under in vitro stimulation with fibrogenic cytokines that are produced in exaggerated quantities in asthmatic airways. A sthma is characterized by chronic airway inflammation and remodeling of the normal bronchial architecture in response to the inflammatory tissue injury (1)(2)(3)(4)(5). The remodeling process has become an important target for therapeutic intervention (3,5) because it may contribute to the chronic sequelae of asthma (6,7), leading to permanently impaired pulmonary function and work disability (8).…”

Section: Identification Of Circulating Fibrocytes As Precursors Of Brmentioning

confidence: 99%

Identification of Circulating Fibrocytes as Precursors of Bronchial Myofibroblasts in Asthma

Schmidt

Sun

Stacey

et al. 2003

The Journal of Immunology

579

623

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The mechanisms contributing to airway wall remodeling in asthma are under investigation to identify appropriate therapeutic targets. Bronchial myofibroblasts would represent an important target because they play a crucial role in the genesis of subepithelial fibrosis, a characteristic feature of the remodeling process, but their origin is poorly understood. We hypothesized that they originate from fibrocytes, circulating cells with the unique characteristic of expressing the hemopoietic stem cell Ag CD34 and collagen I. In this study we show that allergen exposure induces the accumulation of fibrocyte-like cells in the bronchial mucosa of patients with allergic asthma. These cells are CD34-positive; express collagen I and α-smooth muscle actin, a marker of myofibroblasts; and localize to areas of collagen deposition below the epithelium. By tracking labeled circulating fibrocytes in a mouse model of allergic asthma, we provide evidence that fibrocytes are indeed recruited into the bronchial tissue following allergen exposure and differentiate into myofibroblasts. We also show that human circulating fibrocytes acquire the myofibroblast phenotype under in vitro stimulation with fibrogenic cytokines that are produced in exaggerated quantities in asthmatic airways. These results indicate that circulating fibrocytes may function as myofibroblast precursors and may contribute to the genesis of subepithelial fibrosis in asthma.

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Asthma: a disease remodeling the airways

Cited by 243 publications

References 50 publications

Release of transforming growth factor-beta (TGF-β) and fibronectin by alveolar macrophages in airway diseases

Release of transforming growth factor-beta (TGF-β) and fibronectin by alveolar macrophages in airway diseases

Matrix metalloproteinases (MMPs) and tissue inhibitors of MMPs in the respiratory tract: Potential implications in asthma and other lung diseases

Identification of Circulating Fibrocytes as Precursors of Bronchial Myofibroblasts in Asthma

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