PuSH - Publikationsserver des Helmholtz Zentrums München: Genome-wide gene expression analysis reveals unique genes signatures of epithelial reorganization in primary airway epithelium induced by type-I, -II and -III interferons.

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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)

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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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