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10.1159/000366421 http://scihub22266oqcxt.onion/10.1159/000366421 C6738789!6738789!25277143     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       J+Innate+Immun 2015 ; 7 (2): 165-76 Nephropedia Template TP {{tp|p=25277143|t=2015. Interferon-? Inhibits Nonopsonized Phagocytosis of Macrophages via an mTORC1-c/EBP? Pathway |pdf=|usr=}}{{25277143}} gab.com Text Interferon- Inhibits Nonopsonized Phagocytosis of Macrophages via an mTORC1-c/EBP Pathway JO: J Innate Immun http://www.kidney.de/pget.php?&tw=1&pmid=25277143 #FOAvip Bacterial infection often follows virus infection due to pulmonary interferon-? (IFN-?) production during virus infection, which down-regulates macrophage phagocytosis. The molecular mechanisms for this process are still poorly understood. In the present study, IFN-? treatment significantly inhibited the ability of mouse macrophages to phagocytize nonopsonized chicken red blood cells (cRBCs), bacteria and beads in vitro, while it enhanced IgG- and complement-opsonized phagocytosis. IFN-? treatment decreased the expression of MARCO (macrophage receptor with collagenous structure) in macrophages. Macrophages showed lower binding to and phagocytic ability of cRBCs when MARCO was blocked with antibody. In addition, IFN-? induced high activity of mTOR (mammalian target of rapamycin) and decreased the expression of c/EBP? (CCAAT enhancer-binding protein ?) in macrophages. Rapamycin, a specific mTOR inhibitor, significantly reversed the inhibitory effect of IFN-? on nonopsonized phagocytosis of macrophages and restored c/EBP? and MARCO expression. Biochemical assays showed that c/EBP? directly bound to the MARCO gene promoter. Rapamycin significantly hampered the viral-bacterial synergy and protected influenza-infected mice from subsequent bacterial infection. Thus, IFN-? inhibited the nonopsonized phagocytosis of macrophages through the mTOR-c/EBP?-MARCO pathway. The present study offered evidence indicating that mTOR may be one of the key target molecules for the prevention of secondary bacterial infection caused by primary virus infection. Twit Text FOAVip Interferon- Inhibits Nonopsonized Phagocytosis of Macrophages via an mTORC1-c/EBP Pathway ????J Innate Immun http://www.kidney.de/pget.php?&tw=1&pmid=25277143 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25277143 #FOAvip English Wikipedia <ref>{{Cite pmid|25277143}}</ref> Interferon-? Inhibits Nonopsonized Phagocytosis of Macrophages via an mTORC1-c/EBP? Pathway #MMPMID25277143 Wang Z; Zhou S; Sun C; Lei T; Peng J; Li W; Ding P; Lu J; Zhao Y J Innate Immun 2015[Feb]; 7 (2): 165-76 PMID25277143show ga Bacterial infection often follows virus infection due to pulmonary interferon-? (IFN-?) production during virus infection, which down-regulates macrophage phagocytosis. The molecular mechanisms for this process are still poorly understood. In the present study, IFN-? treatment significantly inhibited the ability of mouse macrophages to phagocytize nonopsonized chicken red blood cells (cRBCs), bacteria and beads in vitro, while it enhanced IgG- and complement-opsonized phagocytosis. IFN-? treatment decreased the expression of MARCO (macrophage receptor with collagenous structure) in macrophages. Macrophages showed lower binding to and phagocytic ability of cRBCs when MARCO was blocked with antibody. In addition, IFN-? induced high activity of mTOR (mammalian target of rapamycin) and decreased the expression of c/EBP? (CCAAT enhancer-binding protein ?) in macrophages. Rapamycin, a specific mTOR inhibitor, significantly reversed the inhibitory effect of IFN-? on nonopsonized phagocytosis of macrophages and restored c/EBP? and MARCO expression. Biochemical assays showed that c/EBP? directly bound to the MARCO gene promoter. Rapamycin significantly hampered the viral-bacterial synergy and protected influenza-infected mice from subsequent bacterial infection. Thus, IFN-? inhibited the nonopsonized phagocytosis of macrophages through the mTOR-c/EBP?-MARCO pathway. The present study offered evidence indicating that mTOR may be one of the key target molecules for the prevention of secondary bacterial infection caused by primary virus infection. äInterferon-? Inhibits Nonopsonized Phagocytosis of Macrophages via an (epmc).pdf DeepDyve Pubget Overpricing