Airway Smooth Muscle and Mast Cell–derived CC Chemokine Ligand 19 Mediate Airway Smooth Muscle Migration in Asthma

Kaur, Davinder; Saunders, Ruth; Berger, Patrick; Siddiqui, Salman; Woodman, Lucy; Wardlaw, Andrew J.; Bradding, Peter; Brightling, Christopher E.

doi:10.1164/rccm.200603-394oc

Cited by 130 publications

(133 citation statements)

References 36 publications

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“…Recently, an additional chemokine, fraktalkine (CX 3 CL1), which is increased in asthmatic lung, has been shown to be produced by ASM cells, thereby possibly contributing to mast cell recruitment [25]. Recently, human ASM cells have been reported to express CCR7, while mast cells located within airways of asthmatic patients highly express the ligand for CCR7, CCL19 [29]. Importantly, mast cell-derived CCL19 is reported to induce ASM cell migration and wound repair [29].…”

Section: Asthmamentioning

confidence: 99%

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The mast cell and allergic diseases: role in pathogenesis and implications for therapy

Brown

Wilson

Metcalfe

2007

Clin Experimental Allergy

239

184

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SummaryMast cells have long been recognized for their role in the genesis of allergic inflammation; and more recently for their participation in innate and acquired immune responses. Mast cells reside within tissues including the skin and mucosal membranes, which interface with the external environment; as well as being found within vascularized tissues next to nerves, blood vessels and glandular structures. Mast cells have the capability of reacting both within minutes and over hours to specific stimuli, with local and systemic effects. Mast cells express the high affinity IgE receptor (FceRI) and upon aggregation of FceRI by allergen-specific IgE, mast cells release and generate biologically active preformed and newly synthesized mediators which are involved in many aspects of allergic inflammation. While mast cells have been well documented to be essential for acute allergic reactions, more recently the importance of mast cells in reacting through pattern recognition receptors in innate immune responses has become recognized. Moreover, as our molecular understanding of the mast cell has evolved, novel targets for modulation have been identified with promising therapeutic potential.

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Section: Asthmamentioning

confidence: 99%

“…Recently, human ASM cells have been reported to express CCR7, while mast cells located within airways of asthmatic patients highly express the ligand for CCR7, CCL19 [29]. Importantly, mast cell-derived CCL19 is reported to induce ASM cell migration and wound repair [29].…”

Section: Asthmamentioning

confidence: 99%

The mast cell and allergic diseases: role in pathogenesis and implications for therapy

Brown

Wilson

Metcalfe

2007

Clin Experimental Allergy

239

184

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“…Primary ASM was cultured and characterized as previously described (21). Cells used were passage 2-5.…”

Section: Cell Isolation and Culturementioning

confidence: 99%

“…Primary fibroblasts were isolated from bronchial biopsies, characterized for the fibroblast markers Thy-1 and 1B10 (AbCam, Cambridge, U.K.), and used between passage 6 and 8 (n = 13). The human lung mast cells (HLMCs) were isolated and cultured from nonasthmatic lung (n = 19), as previously described (21). The human mastocytoma cell line (HMC-1) was a generous gift from Dr. J. Butterfield (Mayo Clinic, Rochester, MN), and was cultured as described previously (21).…”

Section: Cell Isolation and Culturementioning

confidence: 99%

Mast Cell Fibroblastoid Differentiation Mediated by Airway Smooth Muscle in Asthma

Kaur

Saunders

Hollins

et al. 2010

The Journal of Immunology

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Mast cell microlocalization to the airway smooth muscle (ASM) bundle is a key feature of asthma, but whether these mast cells have an altered phenotype is uncertain. In this paper, we report that in vivo, mast cells within the ASM bundle, in contrast to mast cells in the bronchial submucosa, commonly expressed fibroblast markers and the number of these cells was closely related to the degree of airway hyperresponsiveness. In vitro human lung mast cells and mast cell lines cultured with fibronectin or with primary human ASM cells acquired typical fibroblastic markers and morphology. This differentiation toward a fibroblastoid phenotype was mediated by ASM-derived extracellular matrix proteins, independent of cell adhesion molecule-1, and was attenuated by α5β1 blockade. Fibroblastoid mast cells demonstrated increased chymase expression and activation with exaggerated spontaneous histamine release. Together these data indicate that in asthma, ASM-derived extracellular matrix proteins mediate human mast cell transition to a fibroblastoid phenotype, suggesting that this may be pivotal in the development of airway dysfunction in asthma.

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“…ASMC were also shown to respond to a wide variety of immune mediators and to express receptors for several noninflammatory cytokines (7). More recently, expression of CCR3, a receptor for a number of C-C chemokines has been described in ASMC (8,9). However, little is known regarding the expression of other relevant C-C chemokine receptors by ASMC.…”

mentioning

confidence: 99%

Expression and Regulation of CCR1 by Airway Smooth Muscle Cells in Asthma

Joubert

Lajoie-Kadoch

Welman

et al. 2008

The Journal of Immunology

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C-C chemokines such as CCL11, CCL5, and CCL3 are central mediators in the pathogenesis of asthma. They are mainly associated with the recruitment and the activation of specific inflammatory cells, such as eosinophils, lymphocytes, and neutrophils. It has recently been shown that they can also activate structural cells, such as airway smooth muscle and epithelial cells. The aims of this study were to examine the expression of the CCL3 receptor, CCR1, on human airway smooth muscle cells (ASMC) and to document the regulation of this receptor by cytokines involved in asthma pathogenesis. We first demonstrated that CCR1 mRNA is increased in the airways of asthmatic vs control subjects and showed for the first time that ASMC express CCR1 mRNA and protein, both in vitro and in vivo. Calcium mobilization by CCR1 ligands confirmed its functionality on ASMC. Stimulation of ASMC with TNF-α and, to a lesser extent, IFN-γ resulted in an up-regulation of CCR1 expression, which was totally suppressed by both dexamethasone or mithramycin. Taken together, our data suggest that CCR1 might be involved in the pathogenesis of asthma, through the activation of ASMC by its ligands.

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Airway Smooth Muscle and Mast Cell–derived CC Chemokine Ligand 19 Mediate Airway Smooth Muscle Migration in Asthma

Abstract: The CCL19/CCR7 axis may play an important role in the development of ASM hyperplasia in asthma.

Cited by 130 publications

References 36 publications

The mast cell and allergic diseases: role in pathogenesis and implications for therapy

The mast cell and allergic diseases: role in pathogenesis and implications for therapy

Mast Cell Fibroblastoid Differentiation Mediated by Airway Smooth Muscle in Asthma

Expression and Regulation of CCR1 by Airway Smooth Muscle Cells in Asthma

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