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10.1016/j.ebiom.2016.07.012 http://scihub22266oqcxt.onion/10.1016/j.ebiom.2016.07.012 C5006695!5006695 !27453322     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27453322 &cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 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 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\27453322 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       EBioMedicine 2016 ; 10 (ä): 204-15 Nephropedia Template TP {{tp|p=27453322 |t=2016. Lactoferrin Suppresses Neutrophil Extracellular Traps Release in Inflammation |pdf=|usr=}}{{27453322 }} gab.com Text Lactoferrin Suppresses Neutrophil Extracellular Traps Release in Inflammation JO: EBioMedicine http://www.kidney.de/pget.php?&tw=1&pmid=27453322 #FOAvip Neutrophils are central players in the innate immune system. They generate neutrophil extracellular traps (NETs), which protect against invading pathogens but are also associated with the development of autoimmune and/or inflammatory diseases and thrombosis. Here, we report that lactoferrin, one of the components of NETs, translocated from the cytoplasm to the plasma membrane and markedly suppressed NETs release. Furthermore, exogenous lactoferrin shrunk the chromatin fibers found in released NETs, without affecting the generation of oxygen radicals, but this failed after chemical removal of the positive charge of lactoferrin, suggesting that charge-charge interactions between lactoferrin and NETs were required for this function. In a model of immune complex-induced NET formation in vivo, intravenous lactoferrin injection markedly reduced the extent of NET formation. These observations suggest that lactoferrin serves as an intrinsic inhibitor of NETs release into the circulation. Thus, lactoferrin may represent a therapeutic lead for controlling NETs release in autoimmune and/or inflammatory diseases. Twit Text FOAVip Lactoferrin Suppresses Neutrophil Extracellular Traps Release in Inflammation ????EBioMedicine http://www.kidney.de/pget.php?&tw=1&pmid=27453322 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27453322 #FOAvip English Wikipedia <ref>{{Cite pmid|27453322 }}</ref> Lactoferrin Suppresses Neutrophil Extracellular Traps Release in Inflammation #MMPMID27453322 Okubo K ; Kamiya M ; Urano Y ; Nishi H ; Herter JM ; Mayadas T ; Hirohama D ; Suzuki K ; Kawakami H ; Tanaka M ; Kurosawa M ; Kagaya S ; Hishikawa K ; Nangaku M ; Fujita T ; Hayashi M ; Hirahashi J EBioMedicine 2016[Aug]; 10 (ä): 204-15 PMID27453322 show ga Neutrophils are central players in the innate immune system. They generate neutrophil extracellular traps (NETs), which protect against invading pathogens but are also associated with the development of autoimmune and/or inflammatory diseases and thrombosis. Here, we report that lactoferrin, one of the components of NETs, translocated from the cytoplasm to the plasma membrane and markedly suppressed NETs release. Furthermore, exogenous lactoferrin shrunk the chromatin fibers found in released NETs, without affecting the generation of oxygen radicals, but this failed after chemical removal of the positive charge of lactoferrin, suggesting that charge-charge interactions between lactoferrin and NETs were required for this function. In a model of immune complex-induced NET formation in vivo, intravenous lactoferrin injection markedly reduced the extent of NET formation. These observations suggest that lactoferrin serves as an intrinsic inhibitor of NETs release into the circulation. Thus, lactoferrin may represent a therapeutic lead for controlling NETs release in autoimmune and/or inflammatory diseases. |Amino Acids [MESH] |Cell Line [MESH] |Cell Membrane/metabolism [MESH] |Extracellular Traps/*metabolism [MESH] |Gene Silencing [MESH] |Histones/metabolism [MESH] |Humans [MESH] |Inflammation/genetics/*immunology/*metabolism [MESH] |Lactoferrin/chemistry/genetics/*metabolism [MESH] |Leukocyte Elastase/metabolism [MESH] |Neutrophils/*metabolism [MESH] |Protein Transport [MESH] |Proteolysis [MESH] |RNA Interference [MESH]Lactoferrin Suppresses Neutrophil Extracellular Traps Release in Infla(epmc).pdf DeepDyve Pubget Overpricing