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dc.contributor.authorMaier, Barbara B
dc.contributor.authorHladik, Anastasiya
dc.contributor.authorLakovits, Karin
dc.contributor.authorKorosec, Ana
dc.contributor.authorMartins, Rui
dc.contributor.authorKral, Julia B
dc.contributor.authorMesteri, Ildiko
dc.contributor.authorStrobl, Birgit
dc.contributor.authorMüller, Mathias
dc.contributor.authorKalinke, Ulrich
dc.contributor.authorMerad, Miriam
dc.contributor.authorKnapp, Sylvia
dc.date.accessioned2018-03-05T15:17:58Z
dc.date.available2018-03-05T15:17:58Z
dc.date.issued2016
dc.identifier.citationType I interferon promotes alveolar epithelial type II cell survival during pulmonary Streptococcus pneumoniae infection and sterile lung injury in mice. 2016, 46 (9):2175-86 Eur. J. Immunol.en
dc.identifier.issn1521-4141
dc.identifier.pmid27312374
dc.identifier.doi10.1002/eji.201546201
dc.identifier.urihttp://hdl.handle.net/10033/621304
dc.description.abstractProtecting the integrity of the lung epithelial barrier is essential to ensure respiration and proper oxygenation in patients suffering from various types of lung inflammation. Type I interferon (IFN-I) has been associated with pulmonary epithelial barrier function, however, the mechanisms and involved cell types remain unknown. We aimed to investigate the importance of IFN-I with respect to its epithelial barrier strengthening function to better understand immune-modulating effects in the lung with potential medical implications. Using a mouse model of pneumococcal pneumonia, we revealed that IFN-I selectively protects alveolar epithelial type II cells (AECII) from inflammation-induced cell death. Mechanistically, signaling via the IFN-I receptor on AECII is sufficient to promote AECII survival. The net effects of IFN-I are barrier protection, together with diminished tissue damage, inflammation, and bacterial loads. Importantly, we found that the protective role of IFN-I can also apply to sterile acute lung injury, in which loss of IFN-I signaling leads to a significant reduction in barrier function caused by AECII cell death. Our data suggest that IFN-I is an important mediator in lung inflammation that plays a protective role by antagonizing inflammation-associated cell obstruction, thereby strengthening the integrity of the epithelial barrier.
dc.language.isoenen
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/*
dc.subject.meshAlveolar Epithelial Cellsen
dc.subject.meshAnimalsen
dc.subject.meshCell Survivalen
dc.subject.meshDisease Models, Animalen
dc.subject.meshFemaleen
dc.subject.meshImmunomodulationen
dc.subject.meshInterferon Type Ien
dc.subject.meshLung Injuryen
dc.subject.meshMacrophages, Alveolaren
dc.subject.meshMiceen
dc.subject.meshMice, Knockouten
dc.subject.meshPneumonia, Pneumococcalen
dc.subject.meshReceptor, Interferon alpha-betaen
dc.subject.meshSignal Transductionen
dc.subject.meshStreptococcus pneumoniaeen
dc.titleType I interferon promotes alveolar epithelial type II cell survival during pulmonary Streptococcus pneumoniae infection and sterile lung injury in mice.en
dc.typeArticleen
dc.contributor.departmentTWINCORE, Zentrum für experimentelle und klinischeInfektionsforschung GmbH, Feodor-Lynen-Str. 7, 30625 Hannover, Germany.en
dc.identifier.journalEuropean journal of immunologyen
refterms.dateFOA2018-06-12T16:50:01Z
html.description.abstractProtecting the integrity of the lung epithelial barrier is essential to ensure respiration and proper oxygenation in patients suffering from various types of lung inflammation. Type I interferon (IFN-I) has been associated with pulmonary epithelial barrier function, however, the mechanisms and involved cell types remain unknown. We aimed to investigate the importance of IFN-I with respect to its epithelial barrier strengthening function to better understand immune-modulating effects in the lung with potential medical implications. Using a mouse model of pneumococcal pneumonia, we revealed that IFN-I selectively protects alveolar epithelial type II cells (AECII) from inflammation-induced cell death. Mechanistically, signaling via the IFN-I receptor on AECII is sufficient to promote AECII survival. The net effects of IFN-I are barrier protection, together with diminished tissue damage, inflammation, and bacterial loads. Importantly, we found that the protective role of IFN-I can also apply to sterile acute lung injury, in which loss of IFN-I signaling leads to a significant reduction in barrier function caused by AECII cell death. Our data suggest that IFN-I is an important mediator in lung inflammation that plays a protective role by antagonizing inflammation-associated cell obstruction, thereby strengthening the integrity of the epithelial barrier.


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