<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Erb A</submitter><funding>Federal Ministry of Education and Research: ESCAPE</funding><funding>Deutsche Forschungsgemeinschaft</funding><funding>German Center of Lung Research (DZL), Comprehensive Pneumology Center (CPC) Munich</funding><funding>German Research Foundation (DFG)</funding><funding>Federal Ministry of Education and Research</funding><pagination>929</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9688329</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>12(11)</volume><pubmed_abstract>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 tig</pubmed_abstract><journal>Biosensors</journal><pubmed_title>Genome-Wide Gene Expression Analysis Reveals Unique Genes Signatures of Epithelial Reorganization in Primary Airway Epithelium Induced by Type-I, -II and -III Interferons.</pubmed_title><pmcid>PMC9688329</pmcid><funding_grant_id>01KI20169A</funding_grant_id><funding_grant_id>398577603</funding_grant_id><pubmed_authors>Schmidt-Weber CB</pubmed_authors><pubmed_authors>Erb A</pubmed_authors><pubmed_authors>Zissler UM</pubmed_authors><pubmed_authors>Chaker AM</pubmed_authors><pubmed_authors>Oelsner M</pubmed_authors><pubmed_authors>Jakwerth CA</pubmed_authors></additional><is_claimable>false</is_claimable><name>Genome-Wide Gene Expression Analysis Reveals Unique Genes Signatures of Epithelial Reorganization in Primary Airway Epithelium Induced by Type-I, -II and -III Interferons.</name><description>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 tig</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Oct</publication><modification>2026-06-21T03:09:38.858Z</modification><creation>2025-04-07T04:19:12.408Z</creation></dates><accession>S-EPMC9688329</accession><cross_references><pubmed>36354438</pubmed><doi>10.3390/bios12110929</doi></cross_references></HashMap>