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10.1038/mi.2016.107 http://scihub22266oqcxt.onion/10.1038/mi.2016.107 C5471142!5471142!27966554     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Mucosal+Immunol 2017 ; 10 (4): 1043-55 Nephropedia Template TP {{tp|p=27966554|t=2017. IL-36 Receptor Deletion Attenuates Lung Injury and Decreases Mortality in Murine Influenza Pneumonia |pdf=|usr=}}{{27966554}} gab.com Text IL-36 Receptor Deletion Attenuates Lung Injury and Decreases Mortality in Murine Influenza Pneumonia JO: Mucosal Immunol http://www.kidney.de/pget.php?&tw=1&pmid=27966554 #FOAvip Influenza virus causes a respiratory disease in human that can progress to lung injury with fatal outcome. The interleukin (IL)-36 cytokines are newly described IL-1 family cytokines that promote inflammatory responses via binding to the IL-36 receptor (IL-36R). The mechanism of expression and the role of IL-36 cytokines is poorly understood. Here, we investigated the role of IL-36 cytokines in modulating the innate inflammatory response during influenza virus-induced pneumonia in mice. The intranasal administration of influenza virus upregulated IL-36? mRNA and protein production in the lungs. In vitro, influenza virus-mediated IL-36? but not IL-36? is induced and secreted from alveolar epithelial cells (AECs) through both a caspase-1 and caspase-3/7 dependent pathway. IL-36? was detected in microparticles shed from AECs and promoted the production of pro-inflammatory cytokines and chemokines in respiratory cells. IL-36R deficient mice were protected from influenza virus-induced lung injury and mortality. Decreased mortality was associated with significantly reduced early accumulation of neutrophils and monocytes/macrophages, activation of lymphocytes, production of pro-inflammatory cytokines and chemokines and permeability of the alveolar-epithelial barrier in despite impaired viral clearance. Taken together, these data indicate that IL-36 ligands exacerbate lung injury during influenza virus infection. Twit Text FOAVip IL-36 Receptor Deletion Attenuates Lung Injury and Decreases Mortality in Murine Influenza Pneumonia ????Mucosal Immunol http://www.kidney.de/pget.php?&tw=1&pmid=27966554 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27966554 #FOAvip English Wikipedia <ref>{{Cite pmid|27966554}}</ref> IL-36 Receptor Deletion Attenuates Lung Injury and Decreases Mortality in Murine Influenza Pneumonia #MMPMID27966554 Aoyagi T; Newstead MW; Zeng X; Kunkel SL; Kaku M; Standiford TJ Mucosal Immunol 2017[Jul]; 10 (4): 1043-55 PMID27966554show ga Influenza virus causes a respiratory disease in human that can progress to lung injury with fatal outcome. The interleukin (IL)-36 cytokines are newly described IL-1 family cytokines that promote inflammatory responses via binding to the IL-36 receptor (IL-36R). The mechanism of expression and the role of IL-36 cytokines is poorly understood. Here, we investigated the role of IL-36 cytokines in modulating the innate inflammatory response during influenza virus-induced pneumonia in mice. The intranasal administration of influenza virus upregulated IL-36? mRNA and protein production in the lungs. In vitro, influenza virus-mediated IL-36? but not IL-36? is induced and secreted from alveolar epithelial cells (AECs) through both a caspase-1 and caspase-3/7 dependent pathway. IL-36? was detected in microparticles shed from AECs and promoted the production of pro-inflammatory cytokines and chemokines in respiratory cells. IL-36R deficient mice were protected from influenza virus-induced lung injury and mortality. Decreased mortality was associated with significantly reduced early accumulation of neutrophils and monocytes/macrophages, activation of lymphocytes, production of pro-inflammatory cytokines and chemokines and permeability of the alveolar-epithelial barrier in despite impaired viral clearance. Taken together, these data indicate that IL-36 ligands exacerbate lung injury during influenza virus infection. äIL-36 Receptor Deletion Attenuates Lung Injury and Decreases Mortality(epmc).pdf DeepDyve Pubget Overpricing