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10.1002/eji.201646792 http://scihub22266oqcxt.onion/10.1002/eji.201646792 C5704912!5704912!28543188     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 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 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 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 302.79999999999995 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\28543188.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Eur+J+Immunol 2017 ; 47 (7): 1188-99 Nephropedia Template TP {{tp|p=28543188|t=2017. CD44 deletion leading to attenuation of experimental autoimmune encephalomyelitis results from alterations in gut microbiome and short-chain fatty acids |pdf=|usr=}}{{28543188}} gab.com Text CD44 deletion leading to attenuation of experimental autoimmune encephalomyelitis results from alterations in gut microbiome and short-chain fatty acids JO: Eur J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=28543188 #FOAvip Dysbiosis in gut microbiome has been shown to be associated with inflammatory and autoimmune diseases. Previous studies from our laboratory demonstrated the pivotal role played by CD44 in the regulation of experimental autoimmune encephalomyelitis (EAE), a murine model of multiple sclerosis (MS). Specifically, we showed that CD44 knockout (KO) mice were resistant to induction of EAE when compared to CD44wildtype (WT) mice and this was due to inhibition in the pro-inflammatory Th1/Th17 cells and increased induction of anti-inflammatory Th2/Treg cells. In the current study, we determined whether these effects resulted from an alteration in gut microbiota and the short-chain fatty acid (SCFA) production in CD44KO mice. Fecal transfer from naïve CD44KO but not CD44WT mice, into EAE-induced CD44WT mice, led to significant amelioration of EAE. High-throughput bacterial 16S rRNA gene sequencing, followed by clustering sequences into operational taxonomic units (OTUs) and biochemical analysis, revealed that EAE-induced CD44KO mice showed significant diversity, richness, and evenness when compared to EAE-induced CD44WT mice at the phylum level, with dominant Bacteroidetes (68.5%) and low Firmicutes (26.8%). Further, data showed a significant change in the abundance of SCFAs, propionic acid and i-butyric acid in EAE-CD44KO compared to EAE-CD44WT mice. In conclusion, our results demonstrate that the attenuation of EAE seen following CD44 gene deletion in mice may result from alterations in the gut microbiota and SCFAs. Furthermore, our studies also demonstrate that the phenotype of gene knock-out animals may be shaped by gut microbiota. Twit Text FOAVip CD44 deletion leading to attenuation of experimental autoimmune encephalomyelitis results from alterations in gut microbiome and short-chain fatty acids ????Eur J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=28543188 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28543188 #FOAvip English Wikipedia <ref>{{Cite pmid|28543188}}</ref> CD44 deletion leading to attenuation of experimental autoimmune encephalomyelitis results from alterations in gut microbiome and short-chain fatty acids #MMPMID28543188 Chitrala KN; Guan H; Singh NP; Busbee B; Gandy A; Mehrpouya-Bahrami P; Ganewatta MS; Tang C; Chatterjee S; Nagarkatti P; Nagarkatti M Eur J Immunol 2017[Jul]; 47 (7): 1188-99 PMID28543188show ga Dysbiosis in gut microbiome has been shown to be associated with inflammatory and autoimmune diseases. Previous studies from our laboratory demonstrated the pivotal role played by CD44 in the regulation of experimental autoimmune encephalomyelitis (EAE), a murine model of multiple sclerosis (MS). Specifically, we showed that CD44 knockout (KO) mice were resistant to induction of EAE when compared to CD44wildtype (WT) mice and this was due to inhibition in the pro-inflammatory Th1/Th17 cells and increased induction of anti-inflammatory Th2/Treg cells. In the current study, we determined whether these effects resulted from an alteration in gut microbiota and the short-chain fatty acid (SCFA) production in CD44KO mice. Fecal transfer from naïve CD44KO but not CD44WT mice, into EAE-induced CD44WT mice, led to significant amelioration of EAE. High-throughput bacterial 16S rRNA gene sequencing, followed by clustering sequences into operational taxonomic units (OTUs) and biochemical analysis, revealed that EAE-induced CD44KO mice showed significant diversity, richness, and evenness when compared to EAE-induced CD44WT mice at the phylum level, with dominant Bacteroidetes (68.5%) and low Firmicutes (26.8%). Further, data showed a significant change in the abundance of SCFAs, propionic acid and i-butyric acid in EAE-CD44KO compared to EAE-CD44WT mice. In conclusion, our results demonstrate that the attenuation of EAE seen following CD44 gene deletion in mice may result from alterations in the gut microbiota and SCFAs. Furthermore, our studies also demonstrate that the phenotype of gene knock-out animals may be shaped by gut microbiota. äCD44 deletion leading to attenuation of experimental autoimmune enceph(epmc).pdf DeepDyve Pubget Overpricing