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10.1681/ASN.2013060653 http://scihub22266oqcxt.onion/10.1681/ASN.2013060653 C4033370!4033370!24525029     free     free     free Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Am+Soc+Nephrol 2014 ; 25 (6): 1163-9 Nephropedia Template TP {{tp|p=24525029|t=2014. Inflammasome Activation by Cystine Crystals: Implications for the Pathogenesis of Cystinosis |pdf=|usr=}}{{24525029}} gab.com Text Inflammasome Activation by Cystine Crystals: Implications for the Pathogenesis of Cystinosis JO: J Am Soc Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=24525029 #FOAvip Intralysosomal cystine crystal accumulation, due to mutations in the CTNS gene, is a hallmark of nephropathic cystinosis, but the role of these crystals in disease pathogenesis remains unclear. We hypothesized that, similar to other host-derived crystalline moieties, cystine crystals can induce IL-1? production through inflammasome activation. Thus, we investigated the proinflammatory effects of cystine crystals in primary human PBMCs. LPS-primed PBMCs stimulated with cystine crystals secreted IL-1? in a dose-dependent manner. Similarly to IL-1? secretion induced by other crystalline inflammasome activators, cystine crystal?induced IL-1? secretion required activation of caspase-1. Additionally, exogenous cystine crystals were internalized by monocytes, and inhibition of phagocytosis, cathepsin B leakage, generation of reactive oxygen species, and potassium efflux reduced cystine crystal?induced IL-1? secretion. Patients with cystinosis had higher levels of circulating IL-1? and IL-18 compared with controls. Analysis of inflammasome-related gene expression in PBMCs from patients with cystinosis revealed a significant increase in IL-1? and CASP-1 transcript levels compared with controls. Moreover, knockout of cystinosin in mice led to significant increases in serum IL-18 levels and kidney expression of inflammasome-related genes (Casp-1, Pycard, Il-18, Il18r1, Il1r1, and Il1rl2). Taken together, these data demonstrate that cystine crystals are endogenous inflammasome-activating stimuli, suggesting a novel role for cystine crystals in the pathogenesis of nephropathic cystinosis. Twit Text FOAVip Inflammasome Activation by Cystine Crystals: Implications for the Pathogenesis of Cystinosis ????J Am Soc Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=24525029 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24525029 #FOAvip English Wikipedia <ref>{{Cite pmid|24525029}}</ref> Inflammasome Activation by Cystine Crystals: Implications for the Pathogenesis of Cystinosis #MMPMID24525029 Prencipe G; Caiello I; Cherqui S; Whisenant T; Petrini S; Emma F; De Benedetti F J Am Soc Nephrol 2014[Jun]; 25 (6): 1163-9 PMID24525029show ga Intralysosomal cystine crystal accumulation, due to mutations in the CTNS gene, is a hallmark of nephropathic cystinosis, but the role of these crystals in disease pathogenesis remains unclear. We hypothesized that, similar to other host-derived crystalline moieties, cystine crystals can induce IL-1? production through inflammasome activation. Thus, we investigated the proinflammatory effects of cystine crystals in primary human PBMCs. LPS-primed PBMCs stimulated with cystine crystals secreted IL-1? in a dose-dependent manner. Similarly to IL-1? secretion induced by other crystalline inflammasome activators, cystine crystal?induced IL-1? secretion required activation of caspase-1. Additionally, exogenous cystine crystals were internalized by monocytes, and inhibition of phagocytosis, cathepsin B leakage, generation of reactive oxygen species, and potassium efflux reduced cystine crystal?induced IL-1? secretion. Patients with cystinosis had higher levels of circulating IL-1? and IL-18 compared with controls. Analysis of inflammasome-related gene expression in PBMCs from patients with cystinosis revealed a significant increase in IL-1? and CASP-1 transcript levels compared with controls. Moreover, knockout of cystinosin in mice led to significant increases in serum IL-18 levels and kidney expression of inflammasome-related genes (Casp-1, Pycard, Il-18, Il18r1, Il1r1, and Il1rl2). Taken together, these data demonstrate that cystine crystals are endogenous inflammasome-activating stimuli, suggesting a novel role for cystine crystals in the pathogenesis of nephropathic cystinosis. äInflammasome Activation by Cystine Crystals: Implications for the Path(epmc).pdf DeepDyve Pubget Overpricing