Type I interferon promotes alveolar epithelial type II cell survival during pulmonary Streptococcus pneumoniae infection and sterile lung injury in mice.
Cast your vote
You can rate an item by clicking the amount of stars they wish to award to this item.
When enough users have cast their vote on this item, the average rating will also be shown.
Your vote was cast
Thank you for your feedback
Thank you for your feedback
AuthorsMaier, Barbara B
Kral, Julia B
MetadataShow full item record
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.
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.
AffiliationTWINCORE, Zentrum für experimentelle und klinischeInfektionsforschung GmbH, Feodor-Lynen-Str. 7, 30625 Hannover, Germany.
JournalEuropean journal of immunology
The following license files are associated with this item:
- Creative Commons
Except where otherwise noted, this item's license is described as http://creativecommons.org/licenses/by-nc-sa/4.0/
- Type I interferon protects against pneumococcal invasive disease by inhibiting bacterial transmigration across the lung.
- Authors: LeMessurier KS, Häcker H, Chi L, Tuomanen E, Redecke V
- Issue date: 2013
- Telomerase reverse transcriptase ameliorates lung fibrosis by protecting alveolar epithelial cells against senescence.
- Authors: Liu T, Gonzalez De Los Santos F, Zhao Y, Wu Z, Rinke AE, Kim KK, Phan SH
- Issue date: 2019 May 31
- Streptococcus pneumoniae stimulates a STING- and IFN regulatory factor 3-dependent type I IFN production in macrophages, which regulates RANTES production in macrophages, cocultured alveolar epithelial cells, and mouse lungs.
- Authors: Koppe U, Högner K, Doehn JM, Müller HC, Witzenrath M, Gutbier B, Bauer S, Pribyl T, Hammerschmidt S, Lohmeyer J, Suttorp N, Herold S, Opitz B
- Issue date: 2012 Jan 15
- Yap/Taz regulate alveolar regeneration and resolution of lung inflammation.
- Authors: LaCanna R, Liccardo D, Zhang P, Tragesser L, Wang Y, Cao T, Chapman HA, Morrisey EE, Shen H, Koch WJ, Kosmider B, Wolfson MR, Tian Y
- Issue date: 2019 Apr 15
- Differential alveolar epithelial injury and protein expression in pneumococcal pneumonia.
- Authors: Tyrrell C, McKechnie SR, Beers MF, Mitchell TJ, McElroy MC
- Issue date: 2012 Jun