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10.1016/j.cell.2008.02.043 http://scihub22266oqcxt.onion/10.1016/j.cell.2008.02.043 18423196!7112336!18423196     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell 2008 ; 133 (2): 235-49 Nephropedia Template TP {{tp|p=18423196|t=2008. Identification of oxidative stress and Toll-like receptor 4 signaling as a key pathway of acute lung injury |pdf=|usr=}}{{18423196}} gab.com Text Identification of oxidative stress and Toll-like receptor 4 signaling as a key pathway of acute lung injury JO: Cell http://www.kidney.de/pget.php?&tw=1&pmid=18423196 #FOAvip Multiple lung pathogens such as chemical agents, H5N1 avian flu, or SARS cause high lethality due to acute respiratory distress syndrome. Here we report that Toll-like receptor 4 (TLR4) mutant mice display natural resistance to acid-induced acute lung injury (ALI). We show that TLR4-TRIF-TRAF6 signaling is a key disease pathway that controls the severity of ALI. The oxidized phospholipid (OxPL) OxPAPC was identified to induce lung injury and cytokine production by lung macrophages via TLR4-TRIF. We observed OxPL production in the lungs of humans and animals infected with SARS, Anthrax, or H5N1. Pulmonary challenge with an inactivated H5N1 avian influenza virus rapidly induces ALI and OxPL formation in mice. Loss of TLR4 or TRIF expression protects mice from H5N1-induced ALI. Moreover, deletion of ncf1, which controls ROS production, improves the severity of H5N1-mediated ALI. Our data identify oxidative stress and innate immunity as key lung injury pathways that control the severity of ALI. Twit Text FOAVip Identification of oxidative stress and Toll-like receptor 4 signaling as a key pathway of acute lung injury ????Cell http://www.kidney.de/pget.php?&tw=1&pmid=18423196 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=18423196 #FOAvip English Wikipedia <ref>{{Cite pmid|18423196}}</ref> Identification of oxidative stress and Toll-like receptor 4 signaling as a key pathway of acute lung injury #MMPMID18423196 Imai Y; Kuba K; Neely GG; Yaghubian-Malhami R; Perkmann T; van Loo G; Ermolaeva M; Veldhuizen R; Leung YH; Wang H; Liu H; Sun Y; Pasparakis M; Kopf M; Mech C; Bavari S; Peiris JS; Slutsky AS; Akira S; Hultqvist M; Holmdahl R; Nicholls J; Jiang C; Binder CJ; Penninger JM Cell 2008[Apr]; 133 (2): 235-49 PMID18423196show ga Multiple lung pathogens such as chemical agents, H5N1 avian flu, or SARS cause high lethality due to acute respiratory distress syndrome. Here we report that Toll-like receptor 4 (TLR4) mutant mice display natural resistance to acid-induced acute lung injury (ALI). We show that TLR4-TRIF-TRAF6 signaling is a key disease pathway that controls the severity of ALI. The oxidized phospholipid (OxPL) OxPAPC was identified to induce lung injury and cytokine production by lung macrophages via TLR4-TRIF. We observed OxPL production in the lungs of humans and animals infected with SARS, Anthrax, or H5N1. Pulmonary challenge with an inactivated H5N1 avian influenza virus rapidly induces ALI and OxPL formation in mice. Loss of TLR4 or TRIF expression protects mice from H5N1-induced ALI. Moreover, deletion of ncf1, which controls ROS production, improves the severity of H5N1-mediated ALI. Our data identify oxidative stress and innate immunity as key lung injury pathways that control the severity of ALI. |*Oxidative Stress[MESH] |Adaptor Proteins, Vesicular Transport/metabolism[MESH] |Animals[MESH] |Humans[MESH] |Influenza, Human/metabolism[MESH] |Interleukin-6/metabolism[MESH] |Lung[MESH] |Mice[MESH] |Mice, Inbred C57BL[MESH] |NADPH Oxidases/metabolism[MESH] |NF-kappa B/metabolism[MESH] |Orthomyxoviridae Infections/metabolism[MESH] |Phospholipids/metabolism[MESH] |Respiratory Distress Syndrome/*metabolism[MESH] |Severe Acute Respiratory Syndrome/metabolism[MESH] |Signal Transduction[MESH]Identification of oxidative stress and Toll-like receptor 4 signaling (epmc).pdf DeepDyve Pubget Overpricing