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10.1128/mBio.00810-19 http://scihub22266oqcxt.onion/10.1128/mBio.00810-19 C6509193!6509193!31064834     free     free     free Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 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\31064834.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       mBio 2019 ; 10 (3): ä Nephropedia Template TP {{tp|p=31064834|t=2019. Influenza ?Trains? the Host for Enhanced Susceptibility to Secondary Bacterial Infection |pdf=|usr=}}{{31064834}} gab.com Text Influenza Trains the Host for Enhanced Susceptibility to Secondary Bacterial Infection JO: mBio http://www.kidney.de/pget.php?&tw=1&pmid=31064834 #FOAvip Enhanced susceptibility to 2° bacterial infections following infection with influenza virus is a global health concern that accounts for many hospitalizations and deaths, particularly during pandemics. The complexity of the impaired host immune response during 2° bacterial infection has been widely studied. Both type I IFN and neutrophil dysfunction through decreased chemokine production have been implicated as mechanisms underlying enhanced susceptibility to 2° bacterial infections. Our findings support the conclusion that selective suppression of CXCL1/CXCL2 represents an IFN-?-mediated ?training? of the macrophage transcriptional response to TLR2 agonists and that blocking of TLR4 therapeutically with Eritoran after influenza virus infection reverses this suppression by blunting influenza-induced IFN-?. Twit Text FOAVip Influenza Trains the Host for Enhanced Susceptibility to Secondary Bacterial Infection ????mBio http://www.kidney.de/pget.php?&tw=1&pmid=31064834 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=31064834 #FOAvip English Wikipedia <ref>{{Cite pmid|31064834}}</ref> Influenza ?Trains? the Host for Enhanced Susceptibility to Secondary Bacterial Infection #MMPMID31064834 Shirey KA; Perkins DJ; Lai W; Zhang W; Fernando LR; Gusovsky F; Blanco JCG; Vogel SN; Arditi M; Kagan J mBio 2019[May]; 10 (3): ä PMID31064834show ga Enhanced susceptibility to 2° bacterial infections following infection with influenza virus is a global health concern that accounts for many hospitalizations and deaths, particularly during pandemics. The complexity of the impaired host immune response during 2° bacterial infection has been widely studied. Both type I IFN and neutrophil dysfunction through decreased chemokine production have been implicated as mechanisms underlying enhanced susceptibility to 2° bacterial infections. Our findings support the conclusion that selective suppression of CXCL1/CXCL2 represents an IFN-?-mediated ?training? of the macrophage transcriptional response to TLR2 agonists and that blocking of TLR4 therapeutically with Eritoran after influenza virus infection reverses this suppression by blunting influenza-induced IFN-?. äInfluenza ?Trains? the Host for Enhanced Susceptibility to Secondary B(epmc).pdf DeepDyve Pubget Overpricing