Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.1371/journal.pntd.0004935 http://scihub22266oqcxt.onion/10.1371/journal.pntd.0004935 C4993389!4993389 !27548618     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 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\27548618 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       PLoS+Negl+Trop+Dis 2016 ; 10 (8 ): e0004935 Nephropedia Template TP {{tp|p=27548618 |t=2016. Liver Necrosis and Lethal Systemic Inflammation in a Murine Model of Rickettsia typhi Infection: Role of Neutrophils, Macrophages and NK Cells |pdf=|usr=}}{{27548618 }} gab.com Text Liver Necrosis and Lethal Systemic Inflammation in a Murine Model of Rickettsia typhi Infection: Role of Neutrophils, Macrophages and NK Cells JO: PLoS Negl Trop Dis http://www.kidney.de/pget.php?&tw=1&pmid=27548618 #FOAvip Rickettsia (R.) typhi is the causative agent of endemic typhus, an emerging febrile disease that is associated with complications such as pneumonia, encephalitis and liver dysfunction. To elucidate how innate immune mechanisms contribute to defense and pathology we here analyzed R. typhi infection of CB17 SCID mice that are congenic to BALB/c mice but lack adaptive immunity. CB17 SCID mice succumbed to R. typhi infection within 21 days and showed high bacterial load in spleen, brain, lung, and liver. Most evident pathological changes in R. typhi-infected CB17 SCID mice were massive liver necrosis and splenomegaly due to the disproportionate accumulation of neutrophils and macrophages (M?). Both neutrophils and M? infiltrated the liver and harbored R. typhi. Both cell populations expressed iNOS and produced reactive oxygen species (ROS) and, thus, exhibited an inflammatory and bactericidal phenotype. Surprisingly, depletion of neutrophils completely prevented liver necrosis but neither altered bacterial load nor protected CB17 SCID mice from death. Furthermore, the absence of neutrophils had no impact on the overwhelming systemic inflammatory response in these mice. This response was predominantly driven by activated M? and NK cells both of which expressed IFN? and is considered as the reason of death. Finally, we observed that iNOS expression by M? and neutrophils did not correlate with R. typhi uptake in vivo. Moreover, we demonstrate that M? hardly respond to R. typhi in vitro. These findings indicate that R. typhi enters M? and also neutrophils unrecognized and that activation of these cells is mediated by other mechanisms in the context of tissue damage in vivo. Twit Text FOAVip Liver Necrosis and Lethal Systemic Inflammation in a Murine Model of Rickettsia typhi Infection: Role of Neutrophils, Macrophages and NK Cells ????PLoS Negl Trop Dis http://www.kidney.de/pget.php?&tw=1&pmid=27548618 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27548618 #FOAvip English Wikipedia <ref>{{Cite pmid|27548618 }}</ref> Liver Necrosis and Lethal Systemic Inflammation in a Murine Model of Rickettsia typhi Infection: Role of Neutrophils, Macrophages and NK Cells #MMPMID27548618 Papp S ; Moderzynski K ; Rauch J ; Heine L ; Kuehl S ; Richardt U ; Mueller H ; Fleischer B ; Osterloh A PLoS Negl Trop Dis 2016[Aug]; 10 (8 ): e0004935 PMID27548618 show ga Rickettsia (R.) typhi is the causative agent of endemic typhus, an emerging febrile disease that is associated with complications such as pneumonia, encephalitis and liver dysfunction. To elucidate how innate immune mechanisms contribute to defense and pathology we here analyzed R. typhi infection of CB17 SCID mice that are congenic to BALB/c mice but lack adaptive immunity. CB17 SCID mice succumbed to R. typhi infection within 21 days and showed high bacterial load in spleen, brain, lung, and liver. Most evident pathological changes in R. typhi-infected CB17 SCID mice were massive liver necrosis and splenomegaly due to the disproportionate accumulation of neutrophils and macrophages (M?). Both neutrophils and M? infiltrated the liver and harbored R. typhi. Both cell populations expressed iNOS and produced reactive oxygen species (ROS) and, thus, exhibited an inflammatory and bactericidal phenotype. Surprisingly, depletion of neutrophils completely prevented liver necrosis but neither altered bacterial load nor protected CB17 SCID mice from death. Furthermore, the absence of neutrophils had no impact on the overwhelming systemic inflammatory response in these mice. This response was predominantly driven by activated M? and NK cells both of which expressed IFN? and is considered as the reason of death. Finally, we observed that iNOS expression by M? and neutrophils did not correlate with R. typhi uptake in vivo. Moreover, we demonstrate that M? hardly respond to R. typhi in vitro. These findings indicate that R. typhi enters M? and also neutrophils unrecognized and that activation of these cells is mediated by other mechanisms in the context of tissue damage in vivo. |Animals [MESH] |Brain/microbiology [MESH] |Cytokines/biosynthesis [MESH] |Disease Models, Animal [MESH] |Immunity, Innate [MESH] |Inflammation/blood/*immunology/microbiology/*pathology [MESH] |Interferon-gamma/biosynthesis [MESH] |Killer Cells, Natural/*immunology [MESH] |Liver/microbiology/*pathology [MESH] |Lung/microbiology [MESH] |Macrophage Activation [MESH] |Macrophages/*immunology [MESH] |Mice [MESH] |Mice, Inbred BALB C [MESH] |Mice, SCID [MESH] |Necrosis [MESH] |Neutrophils/*immunology [MESH] |Nitric Oxide Synthase Type II/biosynthesis [MESH] |Reactive Oxygen Species/metabolism [MESH] |Rickettsia typhi/immunology/pathogenicity [MESH] |Spleen/microbiology/pathology [MESH]Liver Necrosis and Lethal Systemic Inflammation in a Murine Model of R(epmc).pdf DeepDyve Pubget Overpricing