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10.1016/S1473-3099(13)70286-X http://scihub22266oqcxt.onion/10.1016/S1473-3099(13)70286-X 24239327!ä!24239327 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\24239327.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Lancet+Infect+Dis 2014 ; 14 (1): 57-69 Nephropedia Template TP {{tp|p=24239327|t=2014. Pathogenesis of influenza-induced acute respiratory distress syndrome |pdf=|usr=}}{{24239327}} gab.com Text Pathogenesis of influenza-induced acute respiratory distress syndrome JO: Lancet Infect Dis http://www.kidney.de/pget.php?&tw=1&pmid=24239327 #FOAvip Acute respiratory distress syndrome (ARDS) is a fatal complication of influenza infection. In this Review we provide an integrated model for its pathogenesis. ARDS involves damage to the epithelial-endothelial barrier, fluid leakage into the alveolar lumen, and respiratory insufficiency. The most important part of the epithelial-endothelial barrier is the alveolar epithelium, strengthened by tight junctions. Influenza virus targets these epithelial cells, reducing sodium pump activity, damaging tight junctions, and killing infected cells. Infected epithelial cells produce cytokines that attract leucocytes--neutrophils and macrophages--and activate adjacent endothelial cells. Activated endothelial cells and infiltrated leucocytes stimulate further infiltration, and leucocytes induce production of reactive oxygen species and nitric oxide that damage the barrier. Activated macrophages also cause direct apoptosis of epithelial cells. This model for influenza-induced ARDS differs from the classic model, which is centred on endothelial damage, and provides a rationale for therapeutic intervention to moderate host response in influenza-induced ARDS. Twit Text FOAVip Pathogenesis of influenza-induced acute respiratory distress syndrome ????Lancet Infect Dis http://www.kidney.de/pget.php?&tw=1&pmid=24239327 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24239327 #FOAvip English Wikipedia <ref>{{Cite pmid|24239327}}</ref> Pathogenesis of influenza-induced acute respiratory distress syndrome #MMPMID24239327 Short KR; Kroeze EJBV; Fouchier RAM; Kuiken T Lancet Infect Dis 2014[Jan]; 14 (1): 57-69 PMID24239327show ga Acute respiratory distress syndrome (ARDS) is a fatal complication of influenza infection. In this Review we provide an integrated model for its pathogenesis. ARDS involves damage to the epithelial-endothelial barrier, fluid leakage into the alveolar lumen, and respiratory insufficiency. The most important part of the epithelial-endothelial barrier is the alveolar epithelium, strengthened by tight junctions. Influenza virus targets these epithelial cells, reducing sodium pump activity, damaging tight junctions, and killing infected cells. Infected epithelial cells produce cytokines that attract leucocytes--neutrophils and macrophages--and activate adjacent endothelial cells. Activated endothelial cells and infiltrated leucocytes stimulate further infiltration, and leucocytes induce production of reactive oxygen species and nitric oxide that damage the barrier. Activated macrophages also cause direct apoptosis of epithelial cells. This model for influenza-induced ARDS differs from the classic model, which is centred on endothelial damage, and provides a rationale for therapeutic intervention to moderate host response in influenza-induced ARDS. |Endothelial Cells/*pathology/physiology[MESH] |Epithelial Cells/*pathology/physiology/virology[MESH] |Humans[MESH] |Immune System/physiology/physiopathology[MESH] |Influenza, Human/*complications[MESH]Pathogenesis of influenza-induced acute respiratory distress syndrome (epmc).pdf DeepDyve Pubget Overpricing