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10.4049/jimmunol.1202969 http://scihub22266oqcxt.onion/10.4049/jimmunol.1202969 C3679316!3679316!23650615     free     free     free Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 263.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 263.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 263.2 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\23650615.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       J+Immunol 2013 ; 190 (12): 6378-88 Nephropedia Template TP {{tp|p=23650615|t=2013. Inhaled Carbon Monoxide Accelerates Resolution of Inflammation via Unique Pro-Resolving Mediator--Heme Oxygenase-1 Circuits1 |pdf=|usr=}}{{23650615}} gab.com Text Inhaled Carbon Monoxide Accelerates Resolution of Inflammation via Unique Pro-Resolving Mediator--Heme Oxygenase-1 Circuits1 JO: J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=23650615 #FOAvip Resolution of acute inflammation is an active event accompanied by biosynthesis of specialized pro-resolving mediators (SPM). We employed a systems approach to determine the impact of carbon monoxide (CO) in resolution active programs during self-limited inflammation in mice. Compared to ambient air, inhaled CO gas (250 ppm) significantly limited PMN infiltration (~44%, 6h) into peritoneum and shortened resolution interval from 4 to 2 hours. We profiled exudate lipid mediators (LM) via metabololipidomics, CO reduced leukotriene B4 (21±11 vs. 59±24 pg/mouse, 6h) and elevated SPM including resolvin (Rv) D1 (27±4 vs. 16±5 pg/mouse) and maresin 1 (26±9 vs. 15±3 pg/mouse). With human macrophages, SPM (10 pM?10 nM) elevated heme oxygenase (HO)-1 (~50%, 8h). CO also enhanced HO-1 expression and accumulation of RvD1 and RvD5, an action reversed by blockage of a key SPM biosynthesis enzyme 15-lipoxygenase (LOX) type 1. Compared to normoxia, CO increased ~30% phagocytosis of opsonized zymosan with human macrophage, that was further enhanced by SPM (~100%). This CO increased phagocytosis was blocked by 15-LOX inhibition and SPM stimulated phagocytosis was diminished by HO-1 inhibition. In murine peritonitis, both pre-and post-treatment with CO inhalation significantly increased macrophages carrying ingested apoptotic PMN in exudates and enhanced PMN apoptosis. Taken together, these results indicate that CO accelerates resolution of acute inflammation, shortens resolution intervals, enhances macrophage efferocytosis, and temporally regulates local levels of LM/SPM. Moreover, they provide pro-resolving mechanisms for HO-1/CO that is part of the SPM-initiated resolution circuit. Twit Text FOAVip Inhaled Carbon Monoxide Accelerates Resolution of Inflammation via Unique Pro-Resolving Mediator--Heme Oxygenase-1 Circuits1 ????J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=23650615 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=23650615 #FOAvip English Wikipedia <ref>{{Cite pmid|23650615}}</ref> Inhaled Carbon Monoxide Accelerates Resolution of Inflammation via Unique Pro-Resolving Mediator--Heme Oxygenase-1 Circuits1 #MMPMID23650615 Chiang N; Shinohara M; Dalli J; Mirakaj V; Kibi M; Choi AMK; Serhan CN J Immunol 2013[Jun]; 190 (12): 6378-88 PMID23650615show ga Resolution of acute inflammation is an active event accompanied by biosynthesis of specialized pro-resolving mediators (SPM). We employed a systems approach to determine the impact of carbon monoxide (CO) in resolution active programs during self-limited inflammation in mice. Compared to ambient air, inhaled CO gas (250 ppm) significantly limited PMN infiltration (~44%, 6h) into peritoneum and shortened resolution interval from 4 to 2 hours. We profiled exudate lipid mediators (LM) via metabololipidomics, CO reduced leukotriene B4 (21±11 vs. 59±24 pg/mouse, 6h) and elevated SPM including resolvin (Rv) D1 (27±4 vs. 16±5 pg/mouse) and maresin 1 (26±9 vs. 15±3 pg/mouse). With human macrophages, SPM (10 pM?10 nM) elevated heme oxygenase (HO)-1 (~50%, 8h). CO also enhanced HO-1 expression and accumulation of RvD1 and RvD5, an action reversed by blockage of a key SPM biosynthesis enzyme 15-lipoxygenase (LOX) type 1. Compared to normoxia, CO increased ~30% phagocytosis of opsonized zymosan with human macrophage, that was further enhanced by SPM (~100%). This CO increased phagocytosis was blocked by 15-LOX inhibition and SPM stimulated phagocytosis was diminished by HO-1 inhibition. In murine peritonitis, both pre-and post-treatment with CO inhalation significantly increased macrophages carrying ingested apoptotic PMN in exudates and enhanced PMN apoptosis. Taken together, these results indicate that CO accelerates resolution of acute inflammation, shortens resolution intervals, enhances macrophage efferocytosis, and temporally regulates local levels of LM/SPM. Moreover, they provide pro-resolving mechanisms for HO-1/CO that is part of the SPM-initiated resolution circuit. äInhaled Carbon Monoxide Accelerates Resolution of Inflammation via Uni(epmc).pdf DeepDyve Pubget Overpricing