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10.4049/jimmunol.1600702 http://scihub22266oqcxt.onion/10.4049/jimmunol.1600702 C5010928!5010928 !27534554     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27534554 &cmd=llinks): Failed to open stream: HTTP request failed! 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Blood-Borne Lipopolysaccharide Is Rapidly Eliminated by Liver Sinusoidal Endothelial Cells via High-Density Lipoprotein |pdf=|usr=}}{{27534554 }} gab.com Text Blood-Borne Lipopolysaccharide Is Rapidly Eliminated by Liver Sinusoidal Endothelial Cells via High-Density Lipoprotein JO: J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=27534554 #FOAvip During Gram-negative bacterial infections, excessive LPS induces inflammation and sepsis via action on immune cells. However, the bulk of LPS can be cleared from circulation by the liver. Liver clearance is thought to be a slow process mediated exclusively by phagocytic resident macrophages, Kupffer cells (KC). However, we discovered that LPS disappears rapidly from the circulation, with a half-life of 2-4 min in mice, and liver eliminates about three quarters of LPS from blood circulation. Using microscopic techniques, we found that ?75% of fluor-tagged LPS in liver became associated with liver sinusoidal endothelial cells (LSEC) and only ?25% with KC. Notably, the ratio of LSEC-KC-associated LPS remained unchanged 45 min after infusion, indicating that LSEC independently processes the LPS. Most interestingly, results of kinetic analysis of LPS bioactivity, using modified limulus amebocyte lysate assay, suggest that recombinant factor C, an LPS binding protein, competitively inhibits high-density lipoprotein (HDL)-mediated LPS association with LSEC early in the process. Supporting the previous notion, 3 min postinfusion, 75% of infused fluorescently tagged LPS-HDL complex associates with LSEC, suggesting that HDL facilitates LPS clearance. These results lead us to propose a new paradigm of LSEC and HDL in clearing LPS with a potential to avoid inflammation during sepsis. Twit Text FOAVip Blood-Borne Lipopolysaccharide Is Rapidly Eliminated by Liver Sinusoidal Endothelial Cells via High-Density Lipoprotein ????J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=27534554 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27534554 #FOAvip English Wikipedia <ref>{{Cite pmid|27534554 }}</ref> Blood-Borne Lipopolysaccharide Is Rapidly Eliminated by Liver Sinusoidal Endothelial Cells via High-Density Lipoprotein #MMPMID27534554 Yao Z ; Mates JM ; Cheplowitz AM ; Hammer LP ; Maiseyeu A ; Phillips GS ; Wewers MD ; Rajaram MV ; Robinson JM ; Anderson CL ; Ganesan LP J Immunol 2016[Sep]; 197 (6 ): 2390-9 PMID27534554 show ga During Gram-negative bacterial infections, excessive LPS induces inflammation and sepsis via action on immune cells. However, the bulk of LPS can be cleared from circulation by the liver. Liver clearance is thought to be a slow process mediated exclusively by phagocytic resident macrophages, Kupffer cells (KC). However, we discovered that LPS disappears rapidly from the circulation, with a half-life of 2-4 min in mice, and liver eliminates about three quarters of LPS from blood circulation. Using microscopic techniques, we found that ?75% of fluor-tagged LPS in liver became associated with liver sinusoidal endothelial cells (LSEC) and only ?25% with KC. Notably, the ratio of LSEC-KC-associated LPS remained unchanged 45 min after infusion, indicating that LSEC independently processes the LPS. Most interestingly, results of kinetic analysis of LPS bioactivity, using modified limulus amebocyte lysate assay, suggest that recombinant factor C, an LPS binding protein, competitively inhibits high-density lipoprotein (HDL)-mediated LPS association with LSEC early in the process. Supporting the previous notion, 3 min postinfusion, 75% of infused fluorescently tagged LPS-HDL complex associates with LSEC, suggesting that HDL facilitates LPS clearance. These results lead us to propose a new paradigm of LSEC and HDL in clearing LPS with a potential to avoid inflammation during sepsis. |Acute-Phase Proteins/immunology/metabolism [MESH] |Animals [MESH] |Carrier Proteins/immunology/metabolism [MESH] |Endothelial Cells/immunology/*physiology [MESH] |Gram-Negative Bacterial Infections/immunology [MESH] |Half-Life [MESH] |Inflammation/immunology/prevention & control [MESH] |Kinetics [MESH] |Kupffer Cells/immunology [MESH] |Lipopolysaccharides/*blood/immunology/*metabolism [MESH] |Lipoproteins, HDL/immunology/*metabolism [MESH] |Liver/*cytology/immunology [MESH] |Membrane Glycoproteins/immunology/metabolism [MESH] |Mice [MESH]Blood-Borne Lipopolysaccharide Is Rapidly Eliminated by Liver Sinusoid(epmc).pdf DeepDyve Pubget Overpricing