Integrins αvβ5 and αvβ6 Mediate IL-4–induced Collective Migration in Human Airway Epithelial Cells

Lee, Sang-Nam; Ahn, Ji Suk; Lee, Seong Gyu; Lee, Hyung Suk; Choi, Augustine M.K.; Yoon, Joo Heon

doi:10.1165/rcmb.2018-0081oc

Cited by 20 publications

(13 citation statements)

References 44 publications

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“…IL-4, a key mediator in driving and exacerbating allergic inflammation, induced collective migration through integrin αvß5 and αvß6 in well-differentiated HNPE cells (19) . During normal nasal respiration, Solomon et al (16) reported that the nasal air pressure was varied between -30 mmH 2 O and 30 mmH 2 O during normal nasal respiration.…”

Section: Discussionmentioning

confidence: 96%

“…We analysed the cell migration by acquiring the velocity vector field of the migrating NHNE cells and HNPE cells at the apical surface using an open source particle image velocimetry (PIV) analysis software PIVLab (18) written in Matlab (Mathwoks, USA) as described previously (19) .…”

Section: Analysis Of Cell Migrationmentioning

confidence: 99%

“…Transwell-grown HNPE cell layers were processed for immunofluorescence analysis for MUC5AC, acetylated α-tubulin, ZO-1, E-cadherin, and phalloidin using previously described protocols (19) . Images were captured and analysed with confocal laserscanning microscopy (LSM700, Carl Zeiss MicroImaging GmbH, Jena, Germany).…”

Section: Immunofluorescence Stainingmentioning

confidence: 99%

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Compressive stress induces collective migration through cytoskeletal remodelling in nasal polyp epithelium

Chung¹,

Lee²,

Nam³

et al. 2020

Rhin

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Background: Nasal polyps in the nasal cavity and mucous discharge inside the maxillary sinus exhibit compressive stress on the nasal mucosal epithelium. However, there have been only a few studies on how compressive stress impacts the human nasal mucosal epithelium. Methodology: We investigated the effect of compressive stress on collective migration, junctional proteins, transepithelial electrical resistance, epithelial permeability, and gene expression in well-differentiated normal human nasal epithelial (NHNE) cells and human nasal polyp epithelial (HNPE) cells. Results: NHNE cells barely showed collective migration at compressive stress up to 150 mmH 2 0. However, HNPE cells showed much greater degree of collective migration at a lower compressive stress of 100 mmH 2 0. The cell migration of HNPE cells subjected to 100 mmH 2 O compression was significantly decreased at day 3 and was recovered to the status prior to the compressive stress by day 7, indicating that HNPE cells are relatively more sensitive to mechanical pressure than NHNE cells. Compressive stress also increased transepithelial electrical resistance and decreased epithelial permeability, indicating that the compressive stress disturbed the structural organization rather than physical interactions between cells. In addition, we found that compressive stress induced gene expressions relevant to airway inflammation and tissue remodelling in HNPE cells. Conclusion: Taken together, these findings demonstrate that compressive stress on nasal polyp epithelium is capable of inducing collective migration and induce increased expression of genes related to airway inflammation, innate immunity, and polyp remodelling, even in the absence of inflammatory mediators.

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Section: Discussionmentioning

confidence: 96%

Section: Analysis Of Cell Migrationmentioning

confidence: 99%

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Compressive stress induces collective migration through cytoskeletal remodelling in nasal polyp epithelium

Chung¹,

Lee²,

Nam³

et al. 2020

Rhin

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“…Pathologically, ECM remodeling and infiltration of inflammatory cells are closely correlated to eosinophilic asthma, highlighting its potential in the treatment of AR, a condition related to asthma. More recently, literature has emerged providing findings about focal adhesion regulating cell migration in AR . Interestingly, the DEGs in enchondromas were primarily associated with ECM‐receptor interaction, focal adhesion, and amoebiasis as well .…”

Section: Discussionmentioning

confidence: 99%

“…More recently, literature has emerged providing findings about focal adhesion regulating cell migration in AR. 35 Interestingly, the DEGs in enchondromas were primarily associated with ECM-receptor interaction, focal adhesion, and amoebiasis as well. 36 Besides, mucin type O-glycan biosynthesis pathway has been previously reported to be significantly enriched in upregulated miRNAs in chronic rhinosinusitis with nasal polyps use, as per the KEGG database.…”

Section: (A) (B)mentioning

confidence: 98%

Identification of Susceptibility Genes to Allergic Rhinitis by Gene Expression Data Sets

Xue

Yang

Zhao

et al. 2019

Clinical Translational Sci

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As an extremely prevalent disease worldwide, allergic rhinitis (AR) is a condition characterized by chronic inflammation of the nasal mucosa. To identify the finer molecular mechanisms associated with the AR susceptibility genes, differentially expressed genes (DEGs) in AR were investigated. The DEG expression and clinical data of the GSE19187 data set were used for weighted gene co‐expression network analysis (WGCNA). After the modules related to AR had been screened, the genes in the module were extracted for Gene Ontology and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis, whereby the genes enriched in the KEGG pathway were regarded as the pathway‐genes. The DEGs in patients with AR were subsequently screened out from GSE19187, and the sensitive genes were identified in GSE18574 in connection with the allergen challenge. Two kinds of genes were compared with the pathway‐genes in order to screen the AR susceptibility genes. Receiver operating characteristic (ROC) curve was plotted to evaluate the capability of the susceptibility genes to distinguish the AR state. Based on the WGCNA in the GSE19187 data set, 10 co‐expression network modules were identified. The correlation analyses revealed that the yellow module was positively correlated with the disease state of AR. A total of 89 genes were found to be involved in the enrichment of the yellow module pathway. Four genes (CST1, SH2D1B, DPP4, and SLC5A5) were upregulated in AR and sensitive to allergen challenge, whose potentials were further confirmed by ROC curve. Taken together, CST1, SH2D1B, DPP4, and SLC5A5 are susceptibility genes to AR.

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Dupilumab prevents nasal epithelial function alteration by IL‐4 in vitro: Evidence for its efficacy

Fieux,

Carsuzaa,

Bellanger

et al. 2024

Int Forum Allergy Rhinol

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BackgroundChronic rhinosinusitis with nasal polyp (CRSwNP) is a typical type 2 inflammation involving interleukin (IL)‐4 and IL‐13. Dupilumab is a fully human monoclonal antibody targeting IL‐4 receptor α subunit, thereby blocking signaling by both cytokines. Our hypothesis was that IL‐4 and IL‐13, by inducing a severe epithelial dysregulation, are involved in CRSwNP pathogenesis. This study aimed to evaluate the in vitro direct effect of IL‐4, IL‐13, and dupilumab on nasal epithelial functions.MethodsNasal polyps and control mucosa from 28 patients, as well as human nasal epithelial cells (HNEC) from 35 patients with CRSwNP were used. Three major epithelial functions were investigated: the epithelial barrier function (characterized by transepithelial electrical resistance measurements and tight junction protein expression), the ciliary motion (characterized by the ciliary beating efficiency index), and wound healing (characterized by the wound repair rate) under various stimulations (IL‐4, IL‐13, and dupilumab). The main outcome was a significant change in epithelial functions following exposure to IL‐4, IL‐13, and dupilumab for 48 h in the basal media.ResultsIL‐4 (1, 10, and 100 ng/mL) but not IL‐13 induced a significant decrease in occludin and zonula‐occludens protein expression, ciliary beating efficiency, and wound repair rate in HNEC. Dupilumab (0.04 mg/mL) had no effect on HNEC and specifically restored all epithelial functions altered when cells were exposed to a 48‐h IL‐4 stimulation.ConclusionDupilumab, in vitro, restored epithelial integrity by counteracting the effect of IL‐4 on the epithelial barrier (increased epithelial permeability, decreased ciliary beating efficiency, and decreased wound repair rate).

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Integrins α_vβ₅ and α_vβ₆ Mediate IL-4–induced Collective Migration in Human Airway Epithelial Cells

Cited by 20 publications

References 44 publications

Compressive stress induces collective migration through cytoskeletal remodelling in nasal polyp epithelium

Compressive stress induces collective migration through cytoskeletal remodelling in nasal polyp epithelium

Identification of Susceptibility Genes to Allergic Rhinitis by Gene Expression Data Sets

Dupilumab prevents nasal epithelial function alteration by IL‐4 in vitro: Evidence for its efficacy

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