TH17 cytokines induce human airway smooth muscle cell migration

Chang, Ying; Al-Alwan, Laila; Risse, Paul-André; Roussel, Lucie; Rousseau, Stéphane; Halayko, Andrew J.; Martin, James G.; Hamid, Qutayba; Eidelman, David H.

doi:10.1016/j.jaci.2010.12.1117

Cited by 78 publications

(84 citation statements)

References 39 publications

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“…Various stimuli including PDGF-BB, IL-17A/F, and CXCL2 induced ASM cell migration involved in p38 activation (24,32,33). In addition, the current study shows that p38 plays an important role in HB-EGF-induced actin stress fiber disassembly.…”

Section: Discussionsupporting

confidence: 51%

HB-EGF–Promoted Airway Smooth Muscle Cells and Their Progenitor Migration Contribute to Airway Smooth Muscle Remodeling in Asthmatic Mouse

Wang

Yao

et al. 2016

The Journal of Immunology

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The airway smooth muscle (ASM) cells’ proliferation, migration, and their progenitor’s migration are currently regarded as causative factors for ASM remodeling in asthma. Heparin-binding epidermal growth factor (HB-EGF), a potent mitogen and chemotactic factor, could promote ASM cell proliferation through MAPK pathways. In this study, we obtained primary ASM cells and their progenitors from C57BL/6 mice and went on to explore the role of HB-EGF in these cells migration and the underlying mechanisms. We found that recombinant HB-EGF (rHB-EGF) intratracheal instillation accelerated ASM layer thickening in an OVA-induced asthmatic mouse. Modified Boyden chamber assay revealed that rHB-EGF facilitate ASM cell migration in a dose-dependent manner and ASM cells from asthmatic mice had a greater migration ability than that from normal counterparts. rHB-EGF could stimulate the phosphorylation of ERK1/2 and p38 in ASM cells but further migration assay showed that only epidermal growth factor receptor inhibitor (AG1478) or p38 inhibitor (SB203580), but not ERK1/2 inhibitor (PD98059), could inhibit rHB-EGF–mediated ASM cells migration. Actin cytoskeleton experiments exhibited that rHB-EGF could cause actin stress fibers disassembly and focal adhesions formation of ASM cells through the activation of p38. Finally, airway instillation of rHB-EGF promoted the recruitment of bone marrow–derived smooth muscle progenitor cells, which were transferred via caudal vein, migrating into the airway from the circulation. These observations demonstrated that ASM remodeling in asthma might have resulted from HB-EGF–mediated ASM cells and their progenitor cells migration, via p38 MAPK-dependent actin cytoskeleton remodeling.

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Section: Discussionsupporting

confidence: 51%

HB-EGF–Promoted Airway Smooth Muscle Cells and Their Progenitor Migration Contribute to Airway Smooth Muscle Remodeling in Asthmatic Mouse

Wang

Yao

et al. 2016

The Journal of Immunology

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“…In line with an indirect role for IL-17A in bronchoconstriction, CHANG et al [28] originally showed that IL-17A promotes the proliferation and survival of human airway smooth muscle cells in vitro, with a similar relative impact on cells from patients with asthma and control subjects. In further support of an indirect role for IL-17A in bronchoconstriction and/or hyperreactivity, CHANG et al [29] have also shown that IL-17A increases the migration of human airway smooth muscle cells in vitro. Compatible with a more specific role in allergy, SCANLON et al [30] demonstrated that IL-17A stimulates the production of the B-cell chemokine CCL28 in human airway epithelial cells.…”

Section: Other Cells Involved In Asthmamentioning

confidence: 88%

Interleukin-17 cytokine signalling in patients with asthma

Lindén

Dahlén

2014

Eur Respir J

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Asthma remains a global health problem and, therefore, more effective pharmacotherapy is needed. This is particularly true for chronic and severe asthma. In these clinical phenotypes, chronic inflammation involving neutrophils is likely to play a pathogenic role, making it interesting to target cytokine signalling involved in the accumulation of neutrophils. Therefore, it is of interest that the archetype T-helper 17 cell cytokine interleukin (IL)-17A, perhaps also IL-17F, controls neutrophil accumulation, mucus secretion, macrophage mobilisation and smooth muscle reactivity in various experimental airway models. However, much less is known about the involvement of signalling via IL-17 cytokines in humans with asthma. Existing evidence suggests that these cytokines are released from several types of immune cells in asthma and, for IL-17A, there is a local increase associated with disease severity, with the mobilisation of neutrophils and smooth muscle cells locally in the airways. Even though the causative role of IL-17 cytokines remains unclear, there is potential for clinical utility in targeting IL-17A specifically in patients with moderate-to-severe asthma and high reversibility. There is a need for new and well-powered clinical investigations of signalling via IL-17 cytokines in this clinical phenotype. @ERSpublications There is potential utility for drugs targeting IL-17 cytokine signalling in a sub-group of patients with asthma

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“…In recent years, migration of airway smooth muscle cells (ASMCs), including the recruitment of cells with the capacity to differentiate into ASM-like phenotypes (1), has been proposed as a potential mechanism to explain the increase in ASM mass in asthma. Since then, several groups have investigated and established the ability of ASMCs to migrate along a concentration gradient of chemokines (2,3), cytokines (4,5), and other inflammatory mediators (6). Very recently, we published that IL-17 cytokines regulate ASMC migration in an autocrine fashion through production of the growth-related oncogene (GRO) chemokines (GRO-a/CXCL1, GRO-b/CXCL2, GRO-g/ CXCL3) (7), which hereafter are collectively referred to as GROs.…”

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confidence: 99%

Differential Roles of CXCL2 and CXCL3 and Their Receptors in Regulating Normal and Asthmatic Airway Smooth Muscle Cell Migration

Al-Alwan

Chang

Mogas

et al. 2013

The Journal of Immunology

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107

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Structural cell migration plays a central role in the pathophysiology of several diseases, including asthma. Previously, we established that IL-17–induced (CXCL1, CXCL2, and CXCL3) production promoted airway smooth muscle cell (ASMC) migration, and consequently we sought to investigate the molecular mechanism of CXC-induced ASMC migration. Recombinant human CXCL1, CXCL2, and CXCL3 were used to assess migration of human primary ASMCs from normal and asthmatic subjects using a modified Boyden chamber. Neutralizing Abs or small interfering RNA (siRNA) knockdown and pharmacological inhibitors of PI3K, ERK1/2, and p38 MAPK pathways were used to investigate the receptors and the signaling pathways involved in CXC-induced ASMC migration, respectively. We established the ability of CXCL2 and CXCL3, but not CXCL1, to induce ASMC migration at the tested concentrations using normal ASMCs. We found CXCL2-induced ASMC migration to be dependent on p38 MAPK and CXCR2, whereas CXCL3-induced migration was dependent on p38 and ERK1/2 MAPK pathways via CXCR1 and CXCR2. While investigating the effect of CXCL2 and CXCL3 on asthmatic ASMC migration, we found that they induced greater migration of asthmatic ASMCs compared with normal ones. Interestingly, unlike normal ASMCs, CXCL2- and CXCL3-induced asthmatic ASMC migration was mainly mediated by the PI3K pathway through CXCR1. In conclusion, our results establish a new role of CXCR1 in ASMC migration and demonstrate the diverse mechanisms by which CXCL2 and CXCL3 mediate normal and asthmatic ASMC migration, suggesting that they may play a role in the pathogenesis of airway remodeling in asthma.

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TH17 cytokines induce human airway smooth muscle cell migration

Cited by 78 publications

References 39 publications

HB-EGF–Promoted Airway Smooth Muscle Cells and Their Progenitor Migration Contribute to Airway Smooth Muscle Remodeling in Asthmatic Mouse

HB-EGF–Promoted Airway Smooth Muscle Cells and Their Progenitor Migration Contribute to Airway Smooth Muscle Remodeling in Asthmatic Mouse

Interleukin-17 cytokine signalling in patients with asthma

Differential Roles of CXCL2 and CXCL3 and Their Receptors in Regulating Normal and Asthmatic Airway Smooth Muscle Cell Migration

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