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10.1371/journal.pone.0195335 http://scihub22266oqcxt.onion/10.1371/journal.pone.0195335 C5877880!5877880!29601597     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29601597&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 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       PLoS+One 2018 ; 13 (3): ä Nephropedia Template TP {{tp|p=29601597|t=2018. HMGB1/IL-1? complexes in plasma microvesicles modulate immune responses to burn injury |pdf=|usr=}}{{29601597}} gab.com Text HMGB1/IL-1 complexes in plasma microvesicles modulate immune responses to burn injury JO: PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=29601597 #FOAvip Modulating immune responses to sepsis and trauma remain one of the most difficult challenges in modern medicine. Large burn injuries (LBI) are a severe form of trauma associated with sepsis, immune impairment, and mortality. Immune dysfunction after LBI is complex, involving both enhanced and impaired immune activation. The release of Damage-Associated Molecular Patterns (DAMPs), such as HMGB1, and cytokines (e.g. IL-1?) creates an environment of immune dysfunction often leading to end organ failure and death. Both HMGB1 and IL-1? have been found to play critical roles in sepsis and post-burn immune dysfunction. HMGB1 and IL-1? have been shown previously to form potent complexes in vitro. We recently identified the presence of HMGB1/IL-1? heterocomplexes in human tissue. We now find HMGB1/IL-1? complexes in human and mouse plasma, and identify a synergistic role of HMGB1/IL-1? complexes in post-burn immune dysfunction. In both humans and mice, we found that HMGB1 was enriched in plasma microvesicles (MVs) after LBI. HMGB1 was found form complexes with IL-1?. Using flow cytometry of mouse plasma MVs, we identified an increase in an HMGB1+/IL-1?+ MVs. Using co-IP, HMGB1 was found to bind the pro-form of IL-1? in mouse and human plasma. Pro-IL-1?, which is traditionally considered inactive, became active when complexed with HMGB1. Human THP-1 monocytes treated with HMGB1-pro-IL-1? complexes showed increased transcription of LBI associated cytokines IL-6 and IFN? along with suppression of iNOS, mimicking findings associated with LBI. These findings identify that HMGB1/IL-1? complexes released after burn injuries can modulate immune responses, and microvesicles are identified as a novel reservoir for these immune mediators. These complexes might serve as novel immune targets for the treatment of systemic immune responses due to LBI or other causes of sepsis. Twit Text FOAVip HMGB1/IL-1 complexes in plasma microvesicles modulate immune responses to burn injury ????PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=29601597 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29601597 #FOAvip English Wikipedia <ref>{{Cite pmid|29601597}}</ref> HMGB1/IL-1? complexes in plasma microvesicles modulate immune responses to burn injury #MMPMID29601597 Coleman LG; Maile R; Jones SW; Cairns BA; Crews FT PLoS One 2018[]; 13 (3): ä PMID29601597show ga Modulating immune responses to sepsis and trauma remain one of the most difficult challenges in modern medicine. Large burn injuries (LBI) are a severe form of trauma associated with sepsis, immune impairment, and mortality. Immune dysfunction after LBI is complex, involving both enhanced and impaired immune activation. The release of Damage-Associated Molecular Patterns (DAMPs), such as HMGB1, and cytokines (e.g. IL-1?) creates an environment of immune dysfunction often leading to end organ failure and death. Both HMGB1 and IL-1? have been found to play critical roles in sepsis and post-burn immune dysfunction. HMGB1 and IL-1? have been shown previously to form potent complexes in vitro. We recently identified the presence of HMGB1/IL-1? heterocomplexes in human tissue. We now find HMGB1/IL-1? complexes in human and mouse plasma, and identify a synergistic role of HMGB1/IL-1? complexes in post-burn immune dysfunction. In both humans and mice, we found that HMGB1 was enriched in plasma microvesicles (MVs) after LBI. HMGB1 was found form complexes with IL-1?. Using flow cytometry of mouse plasma MVs, we identified an increase in an HMGB1+/IL-1?+ MVs. Using co-IP, HMGB1 was found to bind the pro-form of IL-1? in mouse and human plasma. Pro-IL-1?, which is traditionally considered inactive, became active when complexed with HMGB1. Human THP-1 monocytes treated with HMGB1-pro-IL-1? complexes showed increased transcription of LBI associated cytokines IL-6 and IFN? along with suppression of iNOS, mimicking findings associated with LBI. These findings identify that HMGB1/IL-1? complexes released after burn injuries can modulate immune responses, and microvesicles are identified as a novel reservoir for these immune mediators. These complexes might serve as novel immune targets for the treatment of systemic immune responses due to LBI or other causes of sepsis. äHMGB1/IL-1? complexes in plasma microvesicles modulate immune response(epmc).pdf DeepDyve Pubget Overpricing