%0 Journal Article %1 EJI:EJI3688 %A Maier, B B %A Hladik, A %A Lakovits, K %A Korosec, A %A Martins, R %A Kral, J B %A Mesteri, I %A Strobl, B %A Müller, M %A Kalinke, U %A Merad, M %A Knapp, S %D 2016 %E Immunol, Eur J %J Eur J Immunol %K kalinke %N 9 %P 2175-2186 %T Type I interferon promotes alveolar epithelial type II cell survival during pulmonary Streptococcus pneumoniae infection and sterile lung injury in mice %V 46 %X 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.

@article{EJI:EJI3688, 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.}, added-at = {2016-07-12T09:29:17.000+0200}, author = {Maier, B B and Hladik, A and Lakovits, K and Korosec, A and Martins, R and Kral, J B and Mesteri, I and Strobl, B and Müller, M and Kalinke, U and Merad, M and Knapp, S}, biburl = {https://www.bibsonomy.org/bibtex/28fd80f7149ed36cc67bc6eca743f2390/kalinke}, editor = {Immunol, Eur J}, interhash = {93fe9a48446ccbe10d02343d140f3672}, intrahash = {8fd80f7149ed36cc67bc6eca743f2390}, journal = {Eur J Immunol}, keywords = {kalinke}, number = 9, pages = {2175-2186}, pubmedurl = {http://www.ncbi.nlm.nih.gov/pubmed/27312374}, timestamp = {2016-09-20T11:58:52.000+0200}, title = {Type I interferon promotes alveolar epithelial type II cell survival during pulmonary Streptococcus pneumoniae infection and sterile lung injury in mice}, volume = 46, year = 2016 }