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10.1016/j.jhep.2015.12.020 http://scihub22266oqcxt.onion/10.1016/j.jhep.2015.12.020 C4834232!4834232!26767500     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 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Hepatol 2016 ; 64 (5): 1128-36 Nephropedia Template TP {{tp|p=26767500|t=2016. IL-30 (IL27p28) alleviates sepsis via modulation of cytokine profiles produced by NKT cells |pdf=|usr=}}{{26767500}} gab.com Text IL-30 (IL27p28) alleviates sepsis via modulation of cytokine profiles produced by NKT cells JO: J Hepatol http://www.kidney.de/pget.php?&tw=1&pmid=26767500 #FOAvip Background & Aims: Sepsis is an acute systemic inflammatory response to infection associated with high patient mortality (28-40%). We hypothesized that interleukin (IL)-30, a novel cytokine protecting mice against liver injury resulted from inflammation, would generate a protective effect against systemic inflammation and sepsis-induced death. Methods: Sepsis was induced by lipopolysaccharide (LPS) or cecal ligation and puncture (CLP). The inhibitory effects of IL-30 on septic inflammation and associated therapeutic effects were determined in wild-type, IL-30 (p28)?/?, IL10?/?, and CD1d?/? mice. Results: Mice treated with pIL30 gene therapy or recombinant IL-30 protein (rIL30) were protected from LPS-induced septic shock or CLP-induced polymicrobial sepsis and showed markedly less liver damage and lymphocyte apoptosis than control septic mice. The resulting reduction in mortality was mediated through attenuation of the systemic pro-inflammatory response and augmentation of bacterial clearance. Mice lacking IL-30 were more sensitive to LPS-induced sepsis. Natural killer?like T cells (NKT) produced much higher levels of IL-10 and lower levels of interferon?gamma and tumor necrosis factor?alpha in IL-30?treated septic mice than in control septic mice. Likewise, deficiency in IL-10 or NKT cells abolished the protective role of IL-30 against sepsis. Furthermore, IL-30 induced IL-10 production in purified and LPS-stimulated NKT cells. Blocking IL-6R or gp130 inhibited IL-30 mediated IL-10 production. Conclusions: IL-30 is important in modulating production of NKT cytokines and subsequent NKT cell?mediated immune regulation of other cells. Therefore, IL-30 has a role in prevention and treatment of sepsis via modulation of cytokine production by NKT. Twit Text FOAVip IL-30 (IL27p28) alleviates sepsis via modulation of cytokine profiles produced by NKT cells ????J Hepatol http://www.kidney.de/pget.php?&tw=1&pmid=26767500 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26767500 #FOAvip English Wikipedia <ref>{{Cite pmid|26767500}}</ref> IL-30 (IL27p28) alleviates sepsis via modulation of cytokine profiles produced by NKT cells #MMPMID26767500 Yan J; Mitra A; Hu J; Cutrera JJ; Xia X; Doetschman T; Gagea M; Mishra L; Li S J Hepatol 2016[May]; 64 (5): 1128-36 PMID26767500show ga Background & Aims: Sepsis is an acute systemic inflammatory response to infection associated with high patient mortality (28-40%). We hypothesized that interleukin (IL)-30, a novel cytokine protecting mice against liver injury resulted from inflammation, would generate a protective effect against systemic inflammation and sepsis-induced death. Methods: Sepsis was induced by lipopolysaccharide (LPS) or cecal ligation and puncture (CLP). The inhibitory effects of IL-30 on septic inflammation and associated therapeutic effects were determined in wild-type, IL-30 (p28)?/?, IL10?/?, and CD1d?/? mice. Results: Mice treated with pIL30 gene therapy or recombinant IL-30 protein (rIL30) were protected from LPS-induced septic shock or CLP-induced polymicrobial sepsis and showed markedly less liver damage and lymphocyte apoptosis than control septic mice. The resulting reduction in mortality was mediated through attenuation of the systemic pro-inflammatory response and augmentation of bacterial clearance. Mice lacking IL-30 were more sensitive to LPS-induced sepsis. Natural killer?like T cells (NKT) produced much higher levels of IL-10 and lower levels of interferon?gamma and tumor necrosis factor?alpha in IL-30?treated septic mice than in control septic mice. Likewise, deficiency in IL-10 or NKT cells abolished the protective role of IL-30 against sepsis. Furthermore, IL-30 induced IL-10 production in purified and LPS-stimulated NKT cells. Blocking IL-6R or gp130 inhibited IL-30 mediated IL-10 production. Conclusions: IL-30 is important in modulating production of NKT cytokines and subsequent NKT cell?mediated immune regulation of other cells. Therefore, IL-30 has a role in prevention and treatment of sepsis via modulation of cytokine production by NKT. äIL-30 (IL27p28) alleviates sepsis via modulation of cytokine profiles (epmc).pdf DeepDyve Pubget Overpricing