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10.1172/JCI83931 http://scihub22266oqcxt.onion/10.1172/JCI83931 C4811131!4811131!26999599     free     free     free Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Clin+Invest ä ; 126 (4): 1566-80 Nephropedia Template TP {{tp|p=26999599|t=ä. Macrophage-epithelial paracrine crosstalk inhibits lung edema clearance during influenza infection |pdf=|usr=}}{{26999599}} gab.com Text Macrophage-epithelial paracrine crosstalk inhibits lung edema clearance during influenza infection JO: J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=26999599 #FOAvip Influenza A viruses (IAV) can cause lung injury and acute respiratory distress syndrome (ARDS), which is characterized by accumulation of excessive fluid (edema) in the alveolar airspaces and leads to hypoxemia and death if not corrected. Clearance of excess edema fluid is driven mostly by the alveolar epithelial Na,K-ATPase and is crucial for survival of patients with ARDS. We therefore investigated whether IAV infection alters Na,K-ATPase expression and function in alveolar epithelial cells (AECs) and the ability of the lung to clear edema. IAV infection reduced Na,K-ATPase in the plasma membrane of human and murine AECs and in distal lung epithelium of infected mice. Moreover, induced Na,K-ATPase improved alveolar fluid clearance (AFC) in IAV-infected mice. We identified a paracrine cell communication network between infected and noninfected AECs and alveolar macrophages that leads to decreased alveolar epithelial Na,K-ATPase function and plasma membrane abundance and inhibition of AFC. We determined that the IAV-induced reduction of Na,K-ATPase is mediated by a host signaling pathway that involves epithelial type I IFN and an IFN-dependent elevation of macrophage TNF-related apoptosis?inducing ligand (TRAIL). Our data reveal that interruption of this cellular crosstalk improves edema resolution, which is of biologic and clinical importance to patients with IAV-induced lung injury. Twit Text FOAVip Macrophage-epithelial paracrine crosstalk inhibits lung edema clearance during influenza infection ????J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=26999599 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26999599 #FOAvip English Wikipedia <ref>{{Cite pmid|26999599}}</ref> Macrophage-epithelial paracrine crosstalk inhibits lung edema clearance during influenza infection #MMPMID26999599 Peteranderl C; Morales-Nebreda L; Selvakumar B; Lecuona E; Vadász I; Morty RE; Schmoldt C; Bespalowa J; Wolff T; Pleschka S; Mayer K; Gattenloehner S; Fink L; Lohmeyer J; Seeger W; Sznajder JI; Mutlu GM; Budinger GS; Herold S J Clin Invest ä[]; 126 (4): 1566-80 PMID26999599show ga Influenza A viruses (IAV) can cause lung injury and acute respiratory distress syndrome (ARDS), which is characterized by accumulation of excessive fluid (edema) in the alveolar airspaces and leads to hypoxemia and death if not corrected. Clearance of excess edema fluid is driven mostly by the alveolar epithelial Na,K-ATPase and is crucial for survival of patients with ARDS. We therefore investigated whether IAV infection alters Na,K-ATPase expression and function in alveolar epithelial cells (AECs) and the ability of the lung to clear edema. IAV infection reduced Na,K-ATPase in the plasma membrane of human and murine AECs and in distal lung epithelium of infected mice. Moreover, induced Na,K-ATPase improved alveolar fluid clearance (AFC) in IAV-infected mice. We identified a paracrine cell communication network between infected and noninfected AECs and alveolar macrophages that leads to decreased alveolar epithelial Na,K-ATPase function and plasma membrane abundance and inhibition of AFC. We determined that the IAV-induced reduction of Na,K-ATPase is mediated by a host signaling pathway that involves epithelial type I IFN and an IFN-dependent elevation of macrophage TNF-related apoptosis?inducing ligand (TRAIL). Our data reveal that interruption of this cellular crosstalk improves edema resolution, which is of biologic and clinical importance to patients with IAV-induced lung injury. äMacrophage-epithelial paracrine crosstalk inhibits lung edema clearanc(epmc).pdf DeepDyve Pubget Overpricing