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10.1093/infdis/jir467 http://scihub22266oqcxt.onion/10.1093/infdis/jir467 C3164429!3164429!21881124     free     free     free 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 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 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 Deprecated: Implicit conversion from float 251.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Infect+Dis 2011 ; 204 (7): 1086-94 Nephropedia Template TP {{tp|p=21881124|t=2011. Lowering the Threshold of Lung Innate Immune Cell Activation Alters Susceptibility to Secondary Bacterial Superinfection |pdf=|usr=}}{{21881124}} gab.com Text Lowering the Threshold of Lung Innate Immune Cell Activation Alters Susceptibility to Secondary Bacterial Superinfection JO: J Infect Dis http://www.kidney.de/pget.php?&tw=1&pmid=21881124 #FOAvip Background.?Previous studies have shown that the interaction of CD200R, a myeloid inhibitory receptor, with its ligand, CD200, is critical in the control of innate immune activation in the lung.Methods and Results.?Using a mouse model of bacterial superinfection following influenza, we show that an absence of CD200R (a negative regulator highly expressed by macrophages and dendritic cells), restricts commensal and exogenous bacterial invasiveness and completely prevents the mortality observed in wild-type mice. This benefit is due to a heightened innate immune response to influenza virus in cd200r knockout mice that limits immune pathogenesis and viral load. In wild-type mice, apoptotic cells expressing CD200 that we believe contribute to the suppressed innate immune response to bacteria dominate during the resolution phase of influenza-induced inflammation. We also show for the first time the presence of a variety of previously unidentified bacterial species in the lower airways that are significantly adjusted by influenza virus infection and may contribute to the pathophysiology of disease.Conclusions.?The interaction of CD200 with CD200R therefore contributes to the hyporesponsive innate immune state following influenza virus infection that predisposes to secondary bacterial infection, a phenomenon that has the potential for immune modulation. Twit Text FOAVip Lowering the Threshold of Lung Innate Immune Cell Activation Alters Susceptibility to Secondary Bacterial Superinfection ????J Infect Dis http://www.kidney.de/pget.php?&tw=1&pmid=21881124 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=21881124 #FOAvip English Wikipedia <ref>{{Cite pmid|21881124}}</ref> Lowering the Threshold of Lung Innate Immune Cell Activation Alters Susceptibility to Secondary Bacterial Superinfection #MMPMID21881124 Goulding J; Godlee A; Vekaria S; Hilty M; Snelgrove R; Hussell T J Infect Dis 2011[Oct]; 204 (7): 1086-94 PMID21881124show ga Background.?Previous studies have shown that the interaction of CD200R, a myeloid inhibitory receptor, with its ligand, CD200, is critical in the control of innate immune activation in the lung.Methods and Results.?Using a mouse model of bacterial superinfection following influenza, we show that an absence of CD200R (a negative regulator highly expressed by macrophages and dendritic cells), restricts commensal and exogenous bacterial invasiveness and completely prevents the mortality observed in wild-type mice. This benefit is due to a heightened innate immune response to influenza virus in cd200r knockout mice that limits immune pathogenesis and viral load. In wild-type mice, apoptotic cells expressing CD200 that we believe contribute to the suppressed innate immune response to bacteria dominate during the resolution phase of influenza-induced inflammation. We also show for the first time the presence of a variety of previously unidentified bacterial species in the lower airways that are significantly adjusted by influenza virus infection and may contribute to the pathophysiology of disease.Conclusions.?The interaction of CD200 with CD200R therefore contributes to the hyporesponsive innate immune state following influenza virus infection that predisposes to secondary bacterial infection, a phenomenon that has the potential for immune modulation. äLowering the Threshold of Lung Innate Immune Cell Activation Alters Su(epmc).pdf DeepDyve Pubget Overpricing