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10.1128/IAI.03015-14 http://scihub22266oqcxt.onion/10.1128/IAI.03015-14 C4363445!4363445 !25667262     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 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\25667262 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Infect+Immun 2015 ; 83 (4 ): 1684-94 Nephropedia Template TP {{tp|p=25667262 |t=2015. Role of copper efflux in pneumococcal pathogenesis and resistance to macrophage-mediated immune clearance |pdf=|usr=}}{{25667262 }} gab.com Text Role of copper efflux in pneumococcal pathogenesis and resistance to macrophage-mediated immune clearance JO: Infect Immun http://www.kidney.de/pget.php?&tw=1&pmid=25667262 #FOAvip In bacteria, the intracellular levels of metals are mediated by tightly controlled acquisition and efflux systems. This is particularly true of copper, a trace element that is universally toxic in excess. During infection, the toxic properties of copper are exploited by the mammalian host to facilitate bacterial clearance. To better understand the role of copper during infection, we characterized the contribution of the cop operon to copper homeostasis and virulence in Streptococcus pneumoniae. Deletion of either the exporter, encoded by copA, or the chaperone, encoded by cupA, led to hypersensitivity to copper stress. We further demonstrated that loss of the copper exporter encoded by copA led to decreased virulence in pulmonary, intraperitoneal, and intravenous models of infection. Deletion of copA resulted in enhanced macrophage-mediated bacterial clearance in vitro. The attenuation phenotype of the copA mutant in the lung was found to be dependent on pulmonary macrophages, underscoring the importance of copper efflux in evading immune defenses. Overall, these data provide insight into the role of the cop operon in pneumococcal pathogenesis. Twit Text FOAVip Role of copper efflux in pneumococcal pathogenesis and resistance to macrophage-mediated immune clearance ????Infect Immun http://www.kidney.de/pget.php?&tw=1&pmid=25667262 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25667262 #FOAvip English Wikipedia <ref>{{Cite pmid|25667262 }}</ref> Role of copper efflux in pneumococcal pathogenesis and resistance to macrophage-mediated immune clearance #MMPMID25667262 Johnson MD ; Kehl-Fie TE ; Klein R ; Kelly J ; Burnham C ; Mann B ; Rosch JW Infect Immun 2015[Apr]; 83 (4 ): 1684-94 PMID25667262 show ga In bacteria, the intracellular levels of metals are mediated by tightly controlled acquisition and efflux systems. This is particularly true of copper, a trace element that is universally toxic in excess. During infection, the toxic properties of copper are exploited by the mammalian host to facilitate bacterial clearance. To better understand the role of copper during infection, we characterized the contribution of the cop operon to copper homeostasis and virulence in Streptococcus pneumoniae. Deletion of either the exporter, encoded by copA, or the chaperone, encoded by cupA, led to hypersensitivity to copper stress. We further demonstrated that loss of the copper exporter encoded by copA led to decreased virulence in pulmonary, intraperitoneal, and intravenous models of infection. Deletion of copA resulted in enhanced macrophage-mediated bacterial clearance in vitro. The attenuation phenotype of the copA mutant in the lung was found to be dependent on pulmonary macrophages, underscoring the importance of copper efflux in evading immune defenses. Overall, these data provide insight into the role of the cop operon in pneumococcal pathogenesis. |Animals [MESH] |Bacteremia/genetics/pathology [MESH] |Bacterial Adhesion [MESH] |Bacterial Proteins/*genetics [MESH] |Cation Transport Proteins/*genetics [MESH] |Cell Line [MESH] |Copper/*metabolism [MESH] |Gene Deletion [MESH] |Gene Expression Regulation, Bacterial [MESH] |Humans [MESH] |Lung/immunology/microbiology [MESH] |Macrophages/immunology [MESH] |Mice [MESH] |Mice, Inbred BALB C [MESH] |Molecular Chaperones/metabolism [MESH] |Pneumococcal Infections/genetics/*pathology [MESH]Role of copper efflux in pneumococcal pathogenesis and resistance to (epmc).pdf DeepDyve Pubget Overpricing