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10.1371/journal.ppat.1006582 http://scihub22266oqcxt.onion/10.1371/journal.ppat.1006582 C5589263!5589263 !28841717     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 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 269.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 269.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 269.2 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\28841717 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       PLoS+Pathog 2017 ; 13 (8 ): e1006582 Nephropedia Template TP {{tp|p=28841717 |t=2017. Streptococcus pneumoniae in the heart subvert the host response through biofilm-mediated resident macrophage killing |pdf=|usr=}}{{28841717 }} gab.com Text Streptococcus pneumoniae in the heart subvert the host response through biofilm-mediated resident macrophage killing JO: PLoS Pathog http://www.kidney.de/pget.php?&tw=1&pmid=28841717 #FOAvip For over 130 years, invasive pneumococcal disease has been associated with the presence of extracellular planktonic pneumococci, i.e. diplococci or short chains in affected tissues. Herein, we show that Streptococcus pneumoniae that invade the myocardium instead replicate within cellular vesicles and transition into non-purulent biofilms. Pneumococci within mature cardiac microlesions exhibited salient biofilm features including intrinsic resistance to antibiotic killing and the presence of an extracellular matrix. Dual RNA-seq and subsequent principal component analyses of heart- and blood-isolated pneumococci confirmed the biofilm phenotype in vivo and revealed stark anatomical site-specific differences in virulence gene expression; the latter having major implications on future vaccine antigen selection. Our RNA-seq approach also identified three genomic islands as exclusively expressed in vivo. Deletion of one such island, Region of Diversity 12, resulted in a biofilm-deficient and highly inflammogenic phenotype within the heart; indicating a possible link between the biofilm phenotype and a dampened host-response. We subsequently determined that biofilm pneumococci released greater amounts of the toxin pneumolysin than did planktonic or RD12 deficient pneumococci. This allowed heart-invaded wildtype pneumococci to kill resident cardiac macrophages and subsequently subvert cytokine/chemokine production and neutrophil infiltration into the myocardium. This is the first report for pneumococcal biofilm formation in an invasive disease setting. We show that biofilm pneumococci actively suppress the host response through pneumolysin-mediated immune cell killing. As such, our findings contradict the emerging notion that biofilm pneumococci are passively immunoquiescent. Twit Text FOAVip Streptococcus pneumoniae in the heart subvert the host response through biofilm-mediated resident macrophage killing ????PLoS Pathog http://www.kidney.de/pget.php?&tw=1&pmid=28841717 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28841717 #FOAvip English Wikipedia <ref>{{Cite pmid|28841717 }}</ref> Streptococcus pneumoniae in the heart subvert the host response through biofilm-mediated resident macrophage killing #MMPMID28841717 Shenoy AT ; Brissac T ; Gilley RP ; Kumar N ; Wang Y ; Gonzalez-Juarbe N ; Hinkle WS ; Daugherty SC ; Shetty AC ; Ott S ; Tallon LJ ; Deshane J ; Tettelin H ; Orihuela CJ PLoS Pathog 2017[Aug]; 13 (8 ): e1006582 PMID28841717 show ga For over 130 years, invasive pneumococcal disease has been associated with the presence of extracellular planktonic pneumococci, i.e. diplococci or short chains in affected tissues. Herein, we show that Streptococcus pneumoniae that invade the myocardium instead replicate within cellular vesicles and transition into non-purulent biofilms. Pneumococci within mature cardiac microlesions exhibited salient biofilm features including intrinsic resistance to antibiotic killing and the presence of an extracellular matrix. Dual RNA-seq and subsequent principal component analyses of heart- and blood-isolated pneumococci confirmed the biofilm phenotype in vivo and revealed stark anatomical site-specific differences in virulence gene expression; the latter having major implications on future vaccine antigen selection. Our RNA-seq approach also identified three genomic islands as exclusively expressed in vivo. Deletion of one such island, Region of Diversity 12, resulted in a biofilm-deficient and highly inflammogenic phenotype within the heart; indicating a possible link between the biofilm phenotype and a dampened host-response. We subsequently determined that biofilm pneumococci released greater amounts of the toxin pneumolysin than did planktonic or RD12 deficient pneumococci. This allowed heart-invaded wildtype pneumococci to kill resident cardiac macrophages and subsequently subvert cytokine/chemokine production and neutrophil infiltration into the myocardium. This is the first report for pneumococcal biofilm formation in an invasive disease setting. We show that biofilm pneumococci actively suppress the host response through pneumolysin-mediated immune cell killing. As such, our findings contradict the emerging notion that biofilm pneumococci are passively immunoquiescent. |*Biofilms [MESH] |*Transcriptome [MESH] |Animals [MESH] |Blotting, Western [MESH] |Disease Models, Animal [MESH] |Female [MESH] |Flow Cytometry [MESH] |Fluorescent Antibody Technique [MESH] |Gene Expression Profiling [MESH] |Macrophages/*immunology [MESH] |Mice [MESH] |Mice, Inbred BALB C [MESH] |Microscopy, Electron, Transmission [MESH] |Myocarditis/*immunology/*microbiology [MESH] |Pneumococcal Infections/genetics/*immunology [MESH] |Principal Component Analysis [MESH] |Streptococcus pneumoniae/genetics/immunology [MESH]Streptococcus pneumoniae in the heart subvert the host response throug(epmc).pdf DeepDyve Pubget Overpricing