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10.1016/j.bbadis.2014.08.001 http://scihub22266oqcxt.onion/10.1016/j.bbadis.2014.08.001 C4188733!4188733 !25125050     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 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\25125050 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Biochim+Biophys+Acta 2014 ; 1842 (11 ): 2276-85 Nephropedia Template TP {{tp|p=25125050 |t=2014. Amyloid-?(1-42) protofibrils stimulate a quantum of secreted IL-1? despite significant intracellular IL-1? accumulation in microglia |pdf=|usr=}}{{25125050 }} gab.com Text Amyloid- (1-42) protofibrils stimulate a quantum of secreted IL-1 despite significant intracellular IL-1 accumulation in microglia JO: Biochim Biophys Acta http://www.kidney.de/pget.php?&tw=1&pmid=25125050 #FOAvip Neuroinflammation is a characteristic feature of the Alzheimer's disease (AD) brain. Significant inflammatory markers such as activated microglia and cytokines can be found surrounding the extracellular senile plaques predominantly composed of amyloid-? protein (A?). Several innate immune pathways, including Toll-like receptors (TLRs) and the NLRP3 inflammasome, have been implicated in AD inflammation. A? plays a primary role in activating these pathways which likely contributes to the progressive neurodegeneration in AD. In order to better understand the complexities of this interaction we investigated the inflammatory response of primary microglia to A?(1-42) protofibrils. A?(1-42) protofibrils triggered a time- and MyD88-dependent process that produced tumor necrosis factor alpha (TNF?) and interleukin-1? (IL-1?) mRNA, and intracellular pro and mature forms of IL-1? protein. The accumulation of both IL-1? forms indicated that A?(1-42) protofibrils were able to prime and activate the NLRP3 inflammasome. Surprisingly, A?-induced accumulation of intracellular mature IL-1? did not translate into greater IL-1? secretion. Instead, we found that A? elicited a quantized burst of secreted IL-1? and this process occurred even prior to A? priming of the microglia suggesting a basal level of either pro or mature IL-1? in the cultured primary microglia. The IL-1? secretion burst was rapid but not sustained, yet could be re-evoked with additional A? stimulation. The findings from this study demonstrated multiple sites of IL-1? regulation by A?(1-42) protofibrils including TLR/MyD88-mediated priming, NLRP3 inflammasome activation, and modulation of the IL-1? secretory process. These results underscore the wide-ranging effects of A? on the innate immune response. Twit Text FOAVip Amyloid- (1-42) protofibrils stimulate a quantum of secreted IL-1 despite significant intracellular IL-1 accumulation in microglia ????Biochim Biophys Acta http://www.kidney.de/pget.php?&tw=1&pmid=25125050 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25125050 #FOAvip English Wikipedia <ref>{{Cite pmid|25125050 }}</ref> Amyloid-?(1-42) protofibrils stimulate a quantum of secreted IL-1? despite significant intracellular IL-1? accumulation in microglia #MMPMID25125050 Terrill-Usery SE ; Mohan MJ ; Nichols MR Biochim Biophys Acta 2014[Nov]; 1842 (11 ): 2276-85 PMID25125050 show ga Neuroinflammation is a characteristic feature of the Alzheimer's disease (AD) brain. Significant inflammatory markers such as activated microglia and cytokines can be found surrounding the extracellular senile plaques predominantly composed of amyloid-? protein (A?). Several innate immune pathways, including Toll-like receptors (TLRs) and the NLRP3 inflammasome, have been implicated in AD inflammation. A? plays a primary role in activating these pathways which likely contributes to the progressive neurodegeneration in AD. In order to better understand the complexities of this interaction we investigated the inflammatory response of primary microglia to A?(1-42) protofibrils. A?(1-42) protofibrils triggered a time- and MyD88-dependent process that produced tumor necrosis factor alpha (TNF?) and interleukin-1? (IL-1?) mRNA, and intracellular pro and mature forms of IL-1? protein. The accumulation of both IL-1? forms indicated that A?(1-42) protofibrils were able to prime and activate the NLRP3 inflammasome. Surprisingly, A?-induced accumulation of intracellular mature IL-1? did not translate into greater IL-1? secretion. Instead, we found that A? elicited a quantized burst of secreted IL-1? and this process occurred even prior to A? priming of the microglia suggesting a basal level of either pro or mature IL-1? in the cultured primary microglia. The IL-1? secretion burst was rapid but not sustained, yet could be re-evoked with additional A? stimulation. The findings from this study demonstrated multiple sites of IL-1? regulation by A?(1-42) protofibrils including TLR/MyD88-mediated priming, NLRP3 inflammasome activation, and modulation of the IL-1? secretory process. These results underscore the wide-ranging effects of A? on the innate immune response. äAmyloid-?(1-42) protofibrils stimulate a quantum of secreted IL-1? des(epmc).pdf DeepDyve Pubget Overpricing