Interleukin-8: novel roles in human airway smooth muscle cell contraction and migration

Govindaraju, Vasanthi; Michoud, Marie-Claire; Al-Chalabi, Mustafa; Ferraro, Pasquale; Powell, William S.; Martin, James G.

doi:10.1152/ajpcell.00451.2005

Cited by 121 publications

(103 citation statements)

References 56 publications

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“…We confirmed that CCL5 was a major contributor to the chemotactic activity of HRV-CM for ASMC by demonstrating that incubation of HRV-CM with a specific blocking antibody to CCL5 largely abolished ASMC chemotaxis. Taken together our data are consistent with earlier reports that CCL5 derived from TNFα-stimulated epithelial cells was chemotactic for ASMC (30), and that CXCL8 can also stimulate ASMC migration (25,30).…”

Section: Hrv-induced Asmc Migration Is Mediated At Least In Part VIsupporting

confidence: 93%

Human Rhinovirus Infection of Epithelial Cells Modulates Airway Smooth Muscle Migration

Shariff

Shelfoon

Holden

et al. 2017

Am J Respir Cell Mol Biol

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Rationale: Airway remodeling, a characteristic feature of asthma, begins in early life. Recurrent human rhinovirus (HRV) infections are a potential inciting stimulus for remodeling. One component of airway remodeling is an increase in airway smooth muscle cell mass with a greater proximity of the airway smooth muscle cells (ASMC) to the airway epithelium. We asked whether human bronchial epithelial cells infected with HRV produced mediators that are chemotactic for ASMC.Methods: ASMC migration was investigated using the modified Boyden Chamber and the xCELLigence Real-Time Cell Analyzer. Multiplex bead analysis was used to measure HRVinduced epithelial chemokine release. The chemotactic effects of CCL5, CXCL8 and CXCL10 were also examined.Results: Supernatants from HRV-infected epithelial cells caused ASMC chemotaxis. Pretreatment of ASMC with pertussis toxin abrogated chemotaxis, as did treatment with formoterol, forskolin, or 8-bromo-cAMP. CCL5, CXCL8, and CXCL10 were most up-regulated chemokines produced by HRV-infected airway epithelial cells. When recombinant CCL5, CXCL8 and CXCL10 were used at levels found in epithelial supernatants they induced ASMC chemotaxis similar to that seen with epithelial cell supernatants. When examined individually, CCL5 was the most effective chemokine in causing ASMC migration and treatment of supernatant from HRVinfected epithelial cells with anti-CCL5 antibodies significantly attenuated ASMC migration. Conclusion:These findings suggest that HRV-induced CCL5 can induce ASMC chemotaxis, and thus may contribute to the pathogenesis of airway remodeling in asthmatic patients.3

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Section: Hrv-induced Asmc Migration Is Mediated At Least In Part VIsupporting

confidence: 93%

Human Rhinovirus Infection of Epithelial Cells Modulates Airway Smooth Muscle Migration

Shariff

Shelfoon

Holden

et al. 2017

Am J Respir Cell Mol Biol

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“…TGF-b1 mediates many of its actions by stimulating the release of additional growth factors and inflammatory mediators from airway structural cells. In HASM cells, TGF-b1 stimulates the expression of COX-2 and the release of PGE-2 and IL-8 (118), mediators demonstrated to affect HASM contractile or fibrotic responses (119)(120)(121). In addition, TGF-b1-induced mediator release from the airway epithelium may affect contractile or fibrotic function in HASM cells.…”

Section: Contraction Cell Shortening and Cytoskeletal Motorsmentioning

confidence: 99%

Transforming Growth Factor β1 Function in Airway Remodeling and Hyperresponsiveness. The Missing Link?

Ojiaku

Yoo

Panettieri

2017

Am J Respir Cell Mol Biol

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The pathogenesis of asthma includes a complex interplay among airway inflammation, hyperresponsiveness, and remodeling. Current evidence suggests that airway structural cells, including bronchial smooth muscle cells, myofibroblasts, fibroblasts, and epithelial cells, mediate all three aspects of asthma pathogenesis. Although studies show a connection between airway remodeling and changes in bronchomotor tone, the relationship between the two remains unclear. Transforming growth factor b1 (TGF-b1), a growth factor elevated in the airway of patients with asthma, plays a role in airway remodeling and in the shortening of various airway structural cells. However, the role of TGF-b1 in mediating airway hyperresponsiveness remains unclear. In this review, we summarize the literature addressing the role of TGF-b1 in airway remodeling and shortening. Through our review, we aim to further elucidate the role of TGF-b1 in asthma pathogenesis and the link between airway remodeling and airway hyperresponsiveness in asthma and to define TGF-b1 as a potential therapeutic target for reducing asthma morbidity and mortality.

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“…Human ASMCs were isolated from lung transplant donors and prepared as described previously (32). The protocol was approved by institutional research ethics boards of the McGill University Health Centre and the Université de Montréal, Montreal, QC, Canada and informed consent for ASMC harvesting was obtained at surgery or at the time of lung transplantation.…”

Section: Culture Of Human Asmcsmentioning

confidence: 99%

CXCL1 Inhibits Airway Smooth Muscle Cell Migration through the Decoy Receptor Duffy Antigen Receptor for Chemokines

Al-Alwan

Chang

Rousseau

et al. 2014

The Journal of Immunology

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Airway smooth muscle cell (ASMC) migration is an important mechanism postulated to play a role in airway remodeling in asthma. CXCL1 chemokine has been linked to tissue growth and metastasis. In this study, we present a detailed examination of the inhibitory effect of CXCL1 on human primary ASMC migration and the role of the decoy receptor, Duffy AgR for chemokines (DARC), in this inhibition. Western blots and pathway inhibitors showed that this phenomenon was mediated by activation of the ERK-1/2 MAPK pathway, but not p38 MAPK or PI3K, suggesting a biased selection in the signaling mechanism. Despite being known as a nonsignaling receptor, small interference RNA knockdown of DARC showed that ERK-1/2 MAPK activation was significantly dependent on DARC functionality, which, in turn, was dependent on the presence of heat shock protein 90 subunit α. Interestingly, DARC- or heat shock protein 90 subunit α–deficient ASMCs responded to CXCL1 stimulation by enhancing p38 MAPK activation and ASMC migration through the CXCR2 receptor. In conclusion, we demonstrated DARC’s ability to facilitate CXCL1 inhibition of ASMC migration through modulation of the ERK-1/2 MAPK–signaling pathway.

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Interleukin-8: novel roles in human airway smooth muscle cell contraction and migration

Cited by 121 publications

References 56 publications

Human Rhinovirus Infection of Epithelial Cells Modulates Airway Smooth Muscle Migration

Human Rhinovirus Infection of Epithelial Cells Modulates Airway Smooth Muscle Migration

Transforming Growth Factor β1 Function in Airway Remodeling and Hyperresponsiveness. The Missing Link?

CXCL1 Inhibits Airway Smooth Muscle Cell Migration through the Decoy Receptor Duffy Antigen Receptor for Chemokines

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