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10.1007/s10753-020-01341-7 http://scihub22266oqcxt.onion/10.1007/s10753-020-01341-7 33044666!7548415!33044666     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       Inflammation 2021 ; 44 (1): 358-370 Nephropedia Template TP {{tp|p=33044666|t=2021. Interleukin-1beta Protection Against Experimental Sepsis in Mice |pdf=|usr=}}{{33044666}} gab.com Text Interleukin-1beta Protection Against Experimental Sepsis in Mice JO: Inflammation http://www.kidney.de/pget.php?&tw=1&pmid=33044666 #FOAvip The inflammatory response involving interleukin-1beta (IL-1beta) has been thought to play an important role in the development of late-phase sepsis. However, in this study, we wanted to explore the possibility of using IL-1beta to improve the prognosis of sepsis by triggering local differentiation of bone marrow cells (BMCs) into regulatory dendritic cells (DCs) in vivo, thereby reversing the immune paralysis in late-phase sepsis. Sepsis mouse models were induced by cecal ligation and puncture (CLP) and lethal Escherichia coli O18 infection. Mice were injected intraperitoneally with IL-1beta after CLP and after the lethal infection. Septic BMCs and liver immune cells were isolated at 0, 3, 6, 9, and 14 days post-CLP. BMCs and liver cells isolated from septic mice treated with IL-1beta were adoptively transferred into CLP mice. GFP(+)-C57BL/6 parabiosis models were established. Serum IL-1beta levels were determined by enzyme-linked immunosorbent assay (ELISA) kit, and the number, ratio, and phenotype of immune cells were observed by flow cytometry. IL-1beta treatment improved the survival of sepsis and increased the numbers of BMCs and liver immune cells in septic mice. Moreover, IL-1beta stimulation increased the number and the percentage of CD11c(-)CD45RB(high) DCs in septic BM and liver. Adoptive transfer of septic BMCs, liver immune cells, and CD11c(-)CD45RB(high) DCs treated with IL-1beta into CLP mice attenuated sepsis. IL-1beta triggered the redistribution of CD11c(-)CD45RB(high) DCs as well as BMCs in parabiosis models. IL-1beta protects against sepsis by stimulating local proliferation and differentiation of BMCs into CD11c(-)CD45RB(high) DCs at immune organs and non-immune organs. Twit Text FOAVip Interleukin-1beta Protection Against Experimental Sepsis in Mice ????Inflammation http://www.kidney.de/pget.php?&tw=1&pmid=33044666 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33044666 #FOAvip English Wikipedia <ref>{{Cite pmid|33044666}}</ref> Interleukin-1beta Protection Against Experimental Sepsis in Mice #MMPMID33044666 Guo HL; Shi FD; Zhou Q; Liu QY; Wang YX; Song Y; Wu ZS; Shi YH; Zhang L; Xu KZ; Song GD Inflammation 2021[Feb]; 44 (1): 358-370 PMID33044666show ga The inflammatory response involving interleukin-1beta (IL-1beta) has been thought to play an important role in the development of late-phase sepsis. However, in this study, we wanted to explore the possibility of using IL-1beta to improve the prognosis of sepsis by triggering local differentiation of bone marrow cells (BMCs) into regulatory dendritic cells (DCs) in vivo, thereby reversing the immune paralysis in late-phase sepsis. Sepsis mouse models were induced by cecal ligation and puncture (CLP) and lethal Escherichia coli O18 infection. Mice were injected intraperitoneally with IL-1beta after CLP and after the lethal infection. Septic BMCs and liver immune cells were isolated at 0, 3, 6, 9, and 14 days post-CLP. BMCs and liver cells isolated from septic mice treated with IL-1beta were adoptively transferred into CLP mice. GFP(+)-C57BL/6 parabiosis models were established. Serum IL-1beta levels were determined by enzyme-linked immunosorbent assay (ELISA) kit, and the number, ratio, and phenotype of immune cells were observed by flow cytometry. IL-1beta treatment improved the survival of sepsis and increased the numbers of BMCs and liver immune cells in septic mice. Moreover, IL-1beta stimulation increased the number and the percentage of CD11c(-)CD45RB(high) DCs in septic BM and liver. Adoptive transfer of septic BMCs, liver immune cells, and CD11c(-)CD45RB(high) DCs treated with IL-1beta into CLP mice attenuated sepsis. IL-1beta triggered the redistribution of CD11c(-)CD45RB(high) DCs as well as BMCs in parabiosis models. IL-1beta protects against sepsis by stimulating local proliferation and differentiation of BMCs into CD11c(-)CD45RB(high) DCs at immune organs and non-immune organs. |*Disease Models, Animal[MESH] |Animals[MESH] |Bone Marrow Cells/drug effects/metabolism[MESH] |Cell Movement/drug effects/physiology[MESH] |Dose-Response Relationship, Drug[MESH] |Interleukin-1beta/pharmacology/*therapeutic use[MESH] |Male[MESH] |Mice[MESH] |Mice, Inbred C57BL[MESH]Interleukin-1beta Protection Against Experimental Sepsis in Mice (epmc).pdf DeepDyve Pubget Overpricing