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10.1371/journal.ppat.1003188 http://scihub22266oqcxt.onion/10.1371/journal.ppat.1003188 C3585175!3585175!23468627     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       PLoS+Pathog 2013 ; 9 (2): ä Nephropedia Template TP {{tp|p=23468627|t=2013. Macrophage-expressed IFN-? Contributes to Apoptotic Alveolar Epithelial Cell Injury in Severe Influenza Virus Pneumonia |pdf=|usr=}}{{23468627}} gab.com Text Macrophage-expressed IFN- Contributes to Apoptotic Alveolar Epithelial Cell Injury in Severe Influenza Virus Pneumonia JO: PLoS Pathog http://www.kidney.de/pget.php?&tw=1&pmid=23468627 #FOAvip Influenza viruses (IV) cause pneumonia in humans with progression to lung failure and fatal outcome. Dysregulated release of cytokines including type I interferons (IFNs) has been attributed a crucial role in immune-mediated pulmonary injury during severe IV infection. Using ex vivo and in vivo IV infection models, we demonstrate that alveolar macrophage (AM)-expressed IFN-? significantly contributes to IV-induced alveolar epithelial cell (AEC) injury by autocrine induction of the pro-apoptotic factor TNF-related apoptosis-inducing ligand (TRAIL). Of note, TRAIL was highly upregulated in and released from AM of patients with pandemic H1N1 IV-induced acute lung injury. Elucidating the cell-specific underlying signalling pathways revealed that IV infection induced IFN-? release in AM in a protein kinase R- (PKR-) and NF-?B-dependent way. Bone marrow chimeric mice lacking these signalling mediators in resident and lung-recruited AM and mice subjected to alveolar neutralization of IFN-? and TRAIL displayed reduced alveolar epithelial cell apoptosis and attenuated lung injury during severe IV pneumonia. Together, we demonstrate that macrophage-released type I IFNs, apart from their well-known anti-viral properties, contribute to IV-induced AEC damage and lung injury by autocrine induction of the pro-apoptotic factor TRAIL. Our data suggest that therapeutic targeting of the macrophage IFN-?-TRAIL axis might represent a promising strategy to attenuate IV-induced acute lung injury. Twit Text FOAVip Macrophage-expressed IFN- Contributes to Apoptotic Alveolar Epithelial Cell Injury in Severe Influenza Virus Pneumonia ????PLoS Pathog http://www.kidney.de/pget.php?&tw=1&pmid=23468627 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=23468627 #FOAvip English Wikipedia <ref>{{Cite pmid|23468627}}</ref> Macrophage-expressed IFN-? Contributes to Apoptotic Alveolar Epithelial Cell Injury in Severe Influenza Virus Pneumonia #MMPMID23468627 Högner K; Wolff T; Pleschka S; Plog S; Gruber AD; Kalinke U; Walmrath HD; Bodner J; Gattenlöhner S; Lewe-Schlosser P; Matrosovich M; Seeger W; Lohmeyer J; Herold S PLoS Pathog 2013[Feb]; 9 (2): ä PMID23468627show ga Influenza viruses (IV) cause pneumonia in humans with progression to lung failure and fatal outcome. Dysregulated release of cytokines including type I interferons (IFNs) has been attributed a crucial role in immune-mediated pulmonary injury during severe IV infection. Using ex vivo and in vivo IV infection models, we demonstrate that alveolar macrophage (AM)-expressed IFN-? significantly contributes to IV-induced alveolar epithelial cell (AEC) injury by autocrine induction of the pro-apoptotic factor TNF-related apoptosis-inducing ligand (TRAIL). Of note, TRAIL was highly upregulated in and released from AM of patients with pandemic H1N1 IV-induced acute lung injury. Elucidating the cell-specific underlying signalling pathways revealed that IV infection induced IFN-? release in AM in a protein kinase R- (PKR-) and NF-?B-dependent way. Bone marrow chimeric mice lacking these signalling mediators in resident and lung-recruited AM and mice subjected to alveolar neutralization of IFN-? and TRAIL displayed reduced alveolar epithelial cell apoptosis and attenuated lung injury during severe IV pneumonia. Together, we demonstrate that macrophage-released type I IFNs, apart from their well-known anti-viral properties, contribute to IV-induced AEC damage and lung injury by autocrine induction of the pro-apoptotic factor TRAIL. Our data suggest that therapeutic targeting of the macrophage IFN-?-TRAIL axis might represent a promising strategy to attenuate IV-induced acute lung injury. äMacrophage-expressed IFN-? Contributes to Apoptotic Alveolar Epithelia(epmc).pdf DeepDyve Pubget Overpricing