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10.1371/journal.ppat.1006322 http://scihub22266oqcxt.onion/10.1371/journal.ppat.1006322 C5407765!5407765!28448579     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       PLoS+Pathog 2017 ; 13 (4): ä Nephropedia Template TP {{tp|p=28448579|t=2017. IL-33 receptor ST2 regulates the cognitive impairments associated with experimental cerebral malaria |pdf=|usr=}}{{28448579}} gab.com Text IL-33 receptor ST2 regulates the cognitive impairments associated with experimental cerebral malaria JO: PLoS Pathog http://www.kidney.de/pget.php?&tw=1&pmid=28448579 #FOAvip Cerebral malaria (CM) is associated with a high mortality rate and long-term neurocognitive impairment in survivors. The murine model of experimental cerebral malaria (ECM) induced by Plasmodium berghei ANKA (PbA)-infection reproduces several of these features. We reported recently increased levels of IL-33 protein in brain undergoing ECM and the involvement of IL-33/ST2 pathway in ECM development. Here we show that PbA-infection induced early short term and spatial memory defects, prior to blood brain barrier (BBB) disruption, in wild-type mice, while ST2-deficient mice did not develop cognitive defects. PbA-induced neuroinflammation was reduced in ST2-deficient mice with low Ifng, Tnfa, Il1b, Il6, CXCL9, CXCL10 and Cd8a expression, associated with an absence of neurogenesis defects in hippocampus. PbA-infection triggered a dramatic increase of IL-33 expression by oligodendrocytes, through ST2 pathway. In vitro, IL-33/ST2 pathway induced microglia expression of IL-1? which in turn stimulated IL-33 expression by oligodendrocytes. These results highlight the IL-33/ST2 pathway ability to orchestrate microglia and oligodendrocytes responses at an early stage of PbA-infection, with an amplification loop between IL-1? and IL-33, responsible for an exacerbated neuroinflammation context and associated neurological and cognitive defects. Twit Text FOAVip IL-33 receptor ST2 regulates the cognitive impairments associated with experimental cerebral malaria ????PLoS Pathog http://www.kidney.de/pget.php?&tw=1&pmid=28448579 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28448579 #FOAvip English Wikipedia <ref>{{Cite pmid|28448579}}</ref> IL-33 receptor ST2 regulates the cognitive impairments associated with experimental cerebral malaria #MMPMID28448579 Reverchon F; Mortaud S; Sivoyon M; Maillet I; Laugeray A; Palomo J; Montécot C; Herzine A; Meme S; Meme W; Erard F; Ryffel B; Menuet A; Quesniaux VFJ PLoS Pathog 2017[Apr]; 13 (4): ä PMID28448579show ga Cerebral malaria (CM) is associated with a high mortality rate and long-term neurocognitive impairment in survivors. The murine model of experimental cerebral malaria (ECM) induced by Plasmodium berghei ANKA (PbA)-infection reproduces several of these features. We reported recently increased levels of IL-33 protein in brain undergoing ECM and the involvement of IL-33/ST2 pathway in ECM development. Here we show that PbA-infection induced early short term and spatial memory defects, prior to blood brain barrier (BBB) disruption, in wild-type mice, while ST2-deficient mice did not develop cognitive defects. PbA-induced neuroinflammation was reduced in ST2-deficient mice with low Ifng, Tnfa, Il1b, Il6, CXCL9, CXCL10 and Cd8a expression, associated with an absence of neurogenesis defects in hippocampus. PbA-infection triggered a dramatic increase of IL-33 expression by oligodendrocytes, through ST2 pathway. In vitro, IL-33/ST2 pathway induced microglia expression of IL-1? which in turn stimulated IL-33 expression by oligodendrocytes. These results highlight the IL-33/ST2 pathway ability to orchestrate microglia and oligodendrocytes responses at an early stage of PbA-infection, with an amplification loop between IL-1? and IL-33, responsible for an exacerbated neuroinflammation context and associated neurological and cognitive defects. äIL-33 receptor ST2 regulates the cognitive impairments associated with(epmc).pdf DeepDyve Pubget Overpricing