E-cadherin as an epithelial barrier protein in exhaled breath condensate

Yüksel, Hasan; Türkeli, Ahmet; Taneli, Fatma; Horasan, Gönül Dınç; Kanık, Esra Toprak; Kızılkaya, Metehan; Gözükara, Ceyhun; Yılmaz, Özge

doi:10.1088/1752-7155/8/4/046006

Cited by 12 publications

(9 citation statements)

References 33 publications

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“…In biopsies of the bronchial mucosa of patients with atopic asthma, E-cadherin levels in the respiratory epithelia were shown to be lower than non-atopic and non-asthmatic cases (17,44,45). Similarly, a study published by our group showed that patients with asthma had lower levels of E-cadherin in their airways (46). Similar to previous studies, the present study suggested that E-cadherin and β-catenin levels were lower in asthmatic model mice.…”

Section: Discussionsupporting

confidence: 89%

Anti‑VEGF treatment suppresses remodeling factors and restores epithelial barrier function through the E‑cadherin/β‑catenin signaling axis in experimental asthma models

Türkeli¹,

Yılmaz

Karaman

et al. 2021

Exp Ther Med

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Besides maintaining a physical barrier with adherens junctional (AJ) and tight junctional proteins, airway epithelial cells have important roles in modulating the inflammatory processes of allergic asthma. E-cadherin and β-catenin are the key AJ proteins that are involved in airway remodeling. Various mediators such as transforming growth factor-β (TGF-β), epidermal growth factor (EGF), fibroblast growth factor (FGF), platelet derived growth factor (PDGF), insulin-like growth factor (IGF), tumor necrosis factor-α (TNF-α) and angiogenic factors, such as vascular endothelial growth factor (VEGF), are released by the airway epithelium in allergic asthma. The signaling pathways activated by these growth factors trigger epithelial-mesenchymal transition (EMT), which contributes to fibrosis and subsequent downregulation of E-cadherin. The present study used a mouse asthma model to investigate the effects of anti-VEGF, anti-TNF and corticosteroid therapies on growth factor and E-cadherin/β-catenin expression. The study used 38 male BALB/c mice, divided into 5 groups. A chronic mouse asthma model was created by treating 4 of the groups with inhaled and intraperitoneal ovalbumin (n= 8 per group). Saline, anti-TNF-α (etanercept), anti-VEGF (bevacizumab) or a corticosteroid (dexamethasone) were applied to each group by intraperitoneal injection. No medication was administered to the control group (n=6). Immunohistochemistry for E-cadherin, β-catenin and growth factors was performed on lung tissues and protein expression levels assessed using H-scores. Statistically significant differences were observed in E-cadherin, β-catenin, EGF, FG, and PFGF (P<0.001 for all) as well as the IGF H-scores between the five groups (P<0.005). Only anti-VEGF treatment caused E-cadherin and β-catenin levels to increase to the level of non-asthmatic control groups (P>0.005). All treatment groups had reduced TGF-β, PDGF and FGF H-scores in comparison with the untreated asthma group (P=0.001). The EGF and IGF levels were not significantly different between the untreated asthmatic and non-asthmatic controls. The results suggested that anti-VEGF and TNF-α inhibition treatments are effective in decreasing growth factors, in a similar manner to conventional corticosteroid treatments. Anti-VEGF and TNF inhibition therapy may be an effective treatment for remodeling in asthma while offering an alternative therapeutic option to steroid protective agents. The data suggested that anti-VEGF treatment offered greater restoration of the epithelial barrier than both anti-TNF-α and corticosteroid treatment.

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Section: Discussionsupporting

confidence: 89%

Anti‑VEGF treatment suppresses remodeling factors and restores epithelial barrier function through the E‑cadherin/β‑catenin signaling axis in experimental asthma models

Türkeli¹,

Yılmaz

Karaman

et al. 2021

Exp Ther Med

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“…A variety of allergens and stimuli, except probiotics, are detrimental to the host. After prolonged and/or extensive exposure to ozone, house dust mite (HDM), bacteria and viruses, etc., epithelial structural proteins such as E‐cadherin and zonula occludens‐1 (ZO‐1) were destructed, resulting in decreased epithelial tightness and barrier damage 1‐4 . The dysfunction of epithelia is a common pathological characteristic of mucosal diseases.…”

Section: Mucosal Barrier Acts More Than a Physical Barriermentioning

confidence: 99%

“…After prolonged and/or extensive exposure to ozone, house dust mite (HDM), bacteria and viruses, etc., epithelial structural proteins such as E‐cadherin and zonula occludens‐1 (ZO‐1) were destructed, resulting in decreased epithelial tightness and barrier damage. 1 , 2 , 3 , 4 The dysfunction of epithelia is a common pathological characteristic of mucosal diseases. Various degrees of epithelial damage are the key determinant of mucosal diseases such as asthma, chronic obstructive pulmonary disease (COPD) and inflammatory bowel diseases (IBD) and the degree of epithelial damage is positively correlated with the severity of diseases.…”

Section: Mucosal Barrier Acts More Than a Physical Barriermentioning

confidence: 99%

Innate lymphoid cells are double‐edged swords under the mucosal barrier

Duan

Liu

Lin

et al. 2021

J Cellular Molecular Medi

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As the direct contacting site for pathogens and allergens, the mucosal barrier plays a vital role in the lungs and intestines. Innate lymphoid cells (ILCs) are particularly resident in the mucosal barrier and participate in several pathophysiological processes, such as maintaining or disrupting barrier integrity, preventing various pathogenic invasions. In the pulmonary mucosae, ILCs sometimes aggravate inflammation and mucus hypersecretion but restore airway epithelial integrity and maintain lung tissue homeostasis at other times. In the intestinal mucosae, ILCs can increase epithelial permeability, leading to severe intestinal inflammation on the one hand, and assist mucosal barrier in resisting bacterial invasion on the other hand. In this review, we will illustrate the positive and negative roles of ILCs in mucosal barrier immunity.

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“…This may make the respiratory epithelial cells of asthma patients more sensitive to allergens. 35,36,62,69 In the early 1990s, ultrastructural studies showed that asthmatic patients had fewer intercellular adhesion junction complexes compared with nonasthmatic patients, but the underlying mechanisms of these structural differences remain to be clarified. 18 Disruption of epithelial barrier function has presumed consequences such as easier penetration of inhaled allergens into respiratory tissue, increased allergen access to antigen-presenting cells in the submucosa, and greater extension of spasmogenic agonists to smooth muscles.…”

Section: Asthmamentioning

confidence: 99%

Airway epithelial barrier dysfunction in the pathogenesis and prognosis of respiratory tract diseases in childhood and adulthood

Yüksel

Türkeli

2017

Tissue Barriers

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The lungs are in direct contact with the environment through the tubular structure that constitutes the airway. Starting from the nasal orifice, the airway is exposed to foreign particles including infectious agents, allergens, and other substances that can damage the airways. Therefore, the airway must have a functional epithelial barrier both in the upper and lower airways to protect against these threats. As with the skin, it is likely that the pathogenesis of respiratory diseases is a consequence of epithelial barrier defects in these airways. The characteristics of this system, starting from the beginning of life and extending into maturing and aging, determine the prognosis of respiratory diseases. In this article, we discuss the pathogenesis, clinical phenotype, and prognosis of respiratory diseases from newborns to adulthood in the context of epithelial barrier function and dysfunction.

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E-cadherin as an epithelial barrier protein in exhaled breath condensate

Cited by 12 publications

References 33 publications

Anti‑VEGF treatment suppresses remodeling factors and restores epithelial barrier function through the E‑cadherin/β‑catenin signaling axis in experimental asthma models

Anti‑VEGF treatment suppresses remodeling factors and restores epithelial barrier function through the E‑cadherin/β‑catenin signaling axis in experimental asthma models

Innate lymphoid cells are double‐edged swords under the mucosal barrier

Airway epithelial barrier dysfunction in the pathogenesis and prognosis of respiratory tract diseases in childhood and adulthood

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