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Erb, A. ; Zissler, U.M. ; Oelsner, M. ; Chaker, A. ; Schmidt-Weber, C.B. ; Jakwerth, C.A.

Genome-wide gene expression analysis reveals unique genes signatures of epithelial reorganization in primary airway epithelium induced by type-I, -II and -III interferons.

Biosensors 12:929 (2022)
Verlagsversion Forschungsdaten DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
Biosensors such as toll-like receptors (TLR) induce the expression of interferons (IFNs) after viral infection that are critical to the first step in cell-intrinsic host defense mechanisms. Their differential influence on epithelial integrity genes, however, remains elusive. A genome-wide gene expression biosensor chip for gene expression sensing was used to examine the effects of type-I, -II, and -III IFN stimulation on the epithelial expression profiles of primary organotypic 3D air-liquid interface airway cultures. All types of IFNs induced similar interferon-stimulated genes (ISGs): OAS1, OAS2, and IFIT2. However, they differentially induced transcription factors, epithelial modulators, and pro-inflammatory genes. Type-I IFN-induced genes were associated with cell-cell adhesion and tight junctions, while type-III IFNs promoted genes important for transepithelial transport. In contrast, type-II IFN stimulated proliferation-triggering genes associated and enhanced pro-inflammatory mediator secretion. In conclusion, with our microarray system, we provide evidence that the three IFN types exceed their antiviral ISG-response by inducing distinct remodeling processes, thereby likely strengthening the epithelial airway barrier by enhancing cross-cell-integrity (I), transepithelial transport (III) and finally reconstruction through proliferation (II).
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
Schlagwörter -ii And -iii Interferons ; Airway Epithelial ; Epithelial Integrity ; Gene Expression Analysis ; Microarray ; Remodeling ; Type-i
ISSN (print) / ISBN 2079-6374
e-ISSN 2079-6374
Zeitschrift Biosensors
Quellenangaben Band: 12, Heft: 11, Seiten: , Artikelnummer: 929 Supplement: ,
Verlag MDPI
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed
Institut(e) Institute for Allergy Research (IAF)
Förderungen European Academy of Allergy and Clinical Immunology
Deutsches Zentrum für Lungenforschung
Bundesministerium für Bildung und Forschung
Deutsche Forschungsgemeinschaft
German Center of Lung Research
Comprehensive Pneumology Center