- Title
- Inhibition of β-catenin/CBP signalling improves airway epithelial barrier function and suppresses CCL20 release
- Creator
- Kuchibhotla, Virinchi N. S.; Jonker, Marnix R.; de Bruin, Harold G.; Noordhoek, Jacobien A.; Knight, Darryl A.; Nawijn, Martijn C.; Heijink, Irene H.
- Relation
- Allergy: European Journal of Allergy and Clinical Immunology Vol. 75, Issue 7, p. 1786-1789
- Publisher Link
- http://dx.doi.org/10.1111/all.14216
- Publisher
- Wiley-Blackwell
- Resource Type
- journal article
- Date
- 2020
- Description
- "Letter to the editor: The airway epithelial barrier in asthma may be more susceptible to damage and/or less capable of repair in response to aeroallergens like house dust mite (HDM), resulting in loss of barrier function, as evidenced by reduced expression of cell-cell adhesion protein E-cadherin.1 This may not only lead to increased permeability to allergens and impaired epithelial differentiation, but also result in increased pro-inflammatory responses, including the release of cytokines such as CCL20, GM-CSF, CCL17, IL-33 and TSLP to attract and activate immune cells.2 Epithelial cells from asthma patients display a more basal phenotype than healthy epithelium, along with an inability to re-differentiate into a functionally intact epithelium and reconstitute normal barrier function upon damage by allergens.3 The loss of E-cadherin releases β-catenin, which translocates to the nucleus, inducing divergent gene expression profiles depending on recruitment of different transcriptional co-activators. Recruitment of CREB-binding protein (CBP) results in expression of genes associated with epithelial de-differentiation, migration and proliferation, while p300 induces gene transcription associated with cell differentiation.4 We previously observed that epithelial exposure to HUM results in E-cadherin and β-catenin loss from adherens junctions, accompanied by increased CCL20 release, and that asthma-derived airway epithelial cells are more susceptible to these HDM-induced effects. It is currently unknown whether dysregulated β-catenin signalling contributes to this abnormal epithelial phenotype in asthma."
- Subject
- β-catenin/CBP; airway; asthma; allergens
- Identifier
- http://hdl.handle.net/1959.13/1436617
- Identifier
- uon:40080
- Identifier
- ISSN:0105-4538
- Language
- eng
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