Type I interferon promotes alveolar epithelial type II cell survival during pulmonary Streptococcus pneumoniae infection and sterile lung injury in mice.

2.50
Hdl Handle:
http://hdl.handle.net/10033/621304
Title:
Type I interferon promotes alveolar epithelial type II cell survival during pulmonary Streptococcus pneumoniae infection and sterile lung injury in mice.
Authors:
Maier, Barbara B; Hladik, Anastasiya; Lakovits, Karin; Korosec, Ana; Martins, Rui; Kral, Julia B; Mesteri, Ildiko; Strobl, Birgit; Müller, Mathias; Kalinke, Ulrich ( 0000-0003-0503-9564 ) ; Merad, Miriam; Knapp, Sylvia
Abstract:
Protecting 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.
Affiliation:
TWINCORE, Zentrum für experimentelle und klinischeInfektionsforschung GmbH, Feodor-Lynen-Str. 7, 30625 Hannover, Germany.
Citation:
Type 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.
Journal:
European journal of immunology
Issue Date:
2016
URI:
http://hdl.handle.net/10033/621304
DOI:
10.1002/eji.201546201
PubMed ID:
27312374
Type:
Article
Language:
en
ISSN:
1521-4141
Appears in Collections:
publications of the department of experimental infection research ([TC] EXPI)

Full metadata record

DC FieldValue Language
dc.contributor.authorMaier, Barbara Ben
dc.contributor.authorHladik, Anastasiyaen
dc.contributor.authorLakovits, Karinen
dc.contributor.authorKorosec, Anaen
dc.contributor.authorMartins, Ruien
dc.contributor.authorKral, Julia Ben
dc.contributor.authorMesteri, Ildikoen
dc.contributor.authorStrobl, Birgiten
dc.contributor.authorMüller, Mathiasen
dc.contributor.authorKalinke, Ulrichen
dc.contributor.authorMerad, Miriamen
dc.contributor.authorKnapp, Sylviaen
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.en
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

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