HMGB1 and Histones Play a Significant Role in Inducing Systemic Inflammation and Multiple Organ Dysfunctions in Severe Acute Pancreatitis

Severe acute pancreatitis (SAP) starts as a local inflammation of pancreatic tissue that induces the development of multiple extrapancreatic organs dysfunction; however, the underlying mechanisms are still not clear. Ischemia-reperfusion, circulating inflammatory cytokines, and possible bile cytokin...

Full description

Saved in:
Bibliographic Details
Main Authors: Runkuan Yang, Jyrki Tenhunen, Tor Inge Tonnessen
Format: Article
Language:English
Published: Wiley 2017-01-01
Series:International Journal of Inflammation
Online Access:http://dx.doi.org/10.1155/2017/1817564
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1849308005259018240
author Runkuan Yang
Jyrki Tenhunen
Tor Inge Tonnessen
author_facet Runkuan Yang
Jyrki Tenhunen
Tor Inge Tonnessen
author_sort Runkuan Yang
collection DOAJ
description Severe acute pancreatitis (SAP) starts as a local inflammation of pancreatic tissue that induces the development of multiple extrapancreatic organs dysfunction; however, the underlying mechanisms are still not clear. Ischemia-reperfusion, circulating inflammatory cytokines, and possible bile cytokines significantly contribute to gut mucosal injury and intestinal bacterial translocation (BT) during SAP. Circulating HMGB1 level is significantly increased in SAP patients and HMGB1 is an important factor that mediates (at least partly) gut BT during SAP. Gut BT plays a critical role in triggering/inducing systemic inflammation/sepsis in critical illness, and profound systemic inflammatory response syndrome (SIRS) can lead to multiple organ dysfunction syndrome (MODS) during SAP, and systemic inflammation with multiorgan dysfunction is the cause of death in experimental SAP. Therefore, HMGB1 is an important factor that links gut BT and systemic inflammation. Furthermore, HMGB1 significantly contributes to multiple organ injuries. The SAP patients also have significantly increased circulating histones and cell-free DNAs levels, which can reflect the disease severity and contribute to multiple organ injuries in SAP. Hepatic Kupffer cells (KCs) are the predominant source of circulating inflammatory cytokines in SAP, and new evidence indicates that hepatocyte is another important source of circulating HMGB1 in SAP; therefore, treating the liver injury is important in SAP.
format Article
id doaj-art-1fd5a5f5006249b7b22b9cf79f00cbca
institution Kabale University
issn 2090-8040
2042-0099
language English
publishDate 2017-01-01
publisher Wiley
record_format Article
series International Journal of Inflammation
spelling doaj-art-1fd5a5f5006249b7b22b9cf79f00cbca2025-08-20T03:54:34ZengWileyInternational Journal of Inflammation2090-80402042-00992017-01-01201710.1155/2017/18175641817564HMGB1 and Histones Play a Significant Role in Inducing Systemic Inflammation and Multiple Organ Dysfunctions in Severe Acute PancreatitisRunkuan Yang0Jyrki Tenhunen1Tor Inge Tonnessen2Department of Intensive Care Medicine, Tampere University Hospital, University of Tampere, 10 Biokatu, 33014 Tampere, FinlandDepartment of Intensive Care Medicine, Tampere University Hospital, University of Tampere, 10 Biokatu, 33014 Tampere, FinlandDepartment of Emergencies and Critical Care, Oslo University Hospital, 4950 Nydalen, 0424 Oslo, NorwaySevere acute pancreatitis (SAP) starts as a local inflammation of pancreatic tissue that induces the development of multiple extrapancreatic organs dysfunction; however, the underlying mechanisms are still not clear. Ischemia-reperfusion, circulating inflammatory cytokines, and possible bile cytokines significantly contribute to gut mucosal injury and intestinal bacterial translocation (BT) during SAP. Circulating HMGB1 level is significantly increased in SAP patients and HMGB1 is an important factor that mediates (at least partly) gut BT during SAP. Gut BT plays a critical role in triggering/inducing systemic inflammation/sepsis in critical illness, and profound systemic inflammatory response syndrome (SIRS) can lead to multiple organ dysfunction syndrome (MODS) during SAP, and systemic inflammation with multiorgan dysfunction is the cause of death in experimental SAP. Therefore, HMGB1 is an important factor that links gut BT and systemic inflammation. Furthermore, HMGB1 significantly contributes to multiple organ injuries. The SAP patients also have significantly increased circulating histones and cell-free DNAs levels, which can reflect the disease severity and contribute to multiple organ injuries in SAP. Hepatic Kupffer cells (KCs) are the predominant source of circulating inflammatory cytokines in SAP, and new evidence indicates that hepatocyte is another important source of circulating HMGB1 in SAP; therefore, treating the liver injury is important in SAP.http://dx.doi.org/10.1155/2017/1817564
spellingShingle Runkuan Yang
Jyrki Tenhunen
Tor Inge Tonnessen
HMGB1 and Histones Play a Significant Role in Inducing Systemic Inflammation and Multiple Organ Dysfunctions in Severe Acute Pancreatitis
International Journal of Inflammation
title HMGB1 and Histones Play a Significant Role in Inducing Systemic Inflammation and Multiple Organ Dysfunctions in Severe Acute Pancreatitis
title_full HMGB1 and Histones Play a Significant Role in Inducing Systemic Inflammation and Multiple Organ Dysfunctions in Severe Acute Pancreatitis
title_fullStr HMGB1 and Histones Play a Significant Role in Inducing Systemic Inflammation and Multiple Organ Dysfunctions in Severe Acute Pancreatitis
title_full_unstemmed HMGB1 and Histones Play a Significant Role in Inducing Systemic Inflammation and Multiple Organ Dysfunctions in Severe Acute Pancreatitis
title_short HMGB1 and Histones Play a Significant Role in Inducing Systemic Inflammation and Multiple Organ Dysfunctions in Severe Acute Pancreatitis
title_sort hmgb1 and histones play a significant role in inducing systemic inflammation and multiple organ dysfunctions in severe acute pancreatitis
url http://dx.doi.org/10.1155/2017/1817564
work_keys_str_mv AT runkuanyang hmgb1andhistonesplayasignificantroleininducingsystemicinflammationandmultipleorgandysfunctionsinsevereacutepancreatitis
AT jyrkitenhunen hmgb1andhistonesplayasignificantroleininducingsystemicinflammationandmultipleorgandysfunctionsinsevereacutepancreatitis
AT toringetonnessen hmgb1andhistonesplayasignificantroleininducingsystemicinflammationandmultipleorgandysfunctionsinsevereacutepancreatitis