Abstract
BackgroundHemorrhagic shock and resuscitation (HS/R) can induce multiple organ failure which is associated with high mortality. The lung is an organ commonly affected by the HS/R. Acute lung injury is a major cause of dysfunction in other organ systems. The objective of this study is to test the hypothesis that HS/R causes increased gut permeability which results in induction of high mobility group box1 protein (HMGB1) and further leads to the development of acute lung inflammation.Materials and methodsA mouse model of HS/R was employed in this study. Gut permeability and bacterial translocation were assessed with circulating FD4 and lipopolysaccharide (LPS). Circulating HMGB1 was determined with ELISA. Acute lung inflammation (ALI) was determined with lung myeloperoxidase (MPO) activity and pulmonary protein leakage.ResultsHS/R induced intestinal barrier dysfunction as evidenced by increased circulating FD4 and LPS at 30 min and 2 hrs after resuscitation, respectively. In addition, circulating HMGB1 levels were increased in mice with HS/R as compared with sham animals (p < 0.05). HS/R resulted in ALI (increased lung MPO activity and pulmonary protein leakage in mice with HS/R compared with sham mice, p < 0.05). Inhibition of HMGB1 (A-box and TLR4−/−) attenuated the ALI in mice with HS/R. However, inhibition of HMGB1 did not show protective effect on gut injury in early phase of HS/R in mice.ConclusionsOur results suggest that induction of HMGB1 is important in hemorrhagic shock and resuscitation-induced acute lung inflammation.
Highlights
Traumatic injury is the leading cause of death in people who are under 45 years in the United States
Hemorrhagic shock and resuscitation (HS/R) resulted in Acute lung inflammation (ALI)
Our results suggest that induction of high mobility group box1 protein (HMGB1) is important in hemorrhagic shock and resuscitation-induced acute lung inflammation
Summary
Traumatic injury is the leading cause of death in people who are under 45 years in the United States. Hemorrhagic shock remains to be the leading cause of mortality, accounting for 30-40% of trauma related death. Patients recovering from hemorrhagic shock frequently develop a systemic inflammatory response which can put the patients at risk for multiple organ failure (MOF) [1,2,3]. The injured gut serves to propagate systemic injury during HS/R and initiates the process for induction of MOF [4,5]. Acute lung injury is a major cause of dysfunction in other organ systems. The objective of this study is to test the hypothesis that HS/R causes increased gut permeability which results in induction of high mobility group box protein (HMGB1) and further leads to the development of acute lung inflammation
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