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Induction of acute lung inflammation in mice with hemorrhagic shock and resuscitation: role of HMGB1

BACKGROUND: Hemorrhagic 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 h...

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Autores principales: Kao, Raymond LC, Xu, Xuemei, Xenocostas, Anargyros, Parry, Neil, Mele, Tina, Martin, Claudio M, Rui, Tao
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4193406/
https://www.ncbi.nlm.nih.gov/pubmed/25309129
http://dx.doi.org/10.1186/s12950-014-0030-7
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author Kao, Raymond LC
Xu, Xuemei
Xenocostas, Anargyros
Parry, Neil
Mele, Tina
Martin, Claudio M
Rui, Tao
author_facet Kao, Raymond LC
Xu, Xuemei
Xenocostas, Anargyros
Parry, Neil
Mele, Tina
Martin, Claudio M
Rui, Tao
author_sort Kao, Raymond LC
collection PubMed
description BACKGROUND: Hemorrhagic 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 METHODS: A 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. RESULTS: HS/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. CONCLUSIONS: Our results suggest that induction of HMGB1 is important in hemorrhagic shock and resuscitation-induced acute lung inflammation.
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spelling pubmed-41934062014-10-11 Induction of acute lung inflammation in mice with hemorrhagic shock and resuscitation: role of HMGB1 Kao, Raymond LC Xu, Xuemei Xenocostas, Anargyros Parry, Neil Mele, Tina Martin, Claudio M Rui, Tao J Inflamm (Lond) Research BACKGROUND: Hemorrhagic 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 METHODS: A 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. RESULTS: HS/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. CONCLUSIONS: Our results suggest that induction of HMGB1 is important in hemorrhagic shock and resuscitation-induced acute lung inflammation. BioMed Central 2014-10-08 /pmc/articles/PMC4193406/ /pubmed/25309129 http://dx.doi.org/10.1186/s12950-014-0030-7 Text en © Kao et al.; licensee BioMed Central Ltd. 2014 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Research
Kao, Raymond LC
Xu, Xuemei
Xenocostas, Anargyros
Parry, Neil
Mele, Tina
Martin, Claudio M
Rui, Tao
Induction of acute lung inflammation in mice with hemorrhagic shock and resuscitation: role of HMGB1
title Induction of acute lung inflammation in mice with hemorrhagic shock and resuscitation: role of HMGB1
title_full Induction of acute lung inflammation in mice with hemorrhagic shock and resuscitation: role of HMGB1
title_fullStr Induction of acute lung inflammation in mice with hemorrhagic shock and resuscitation: role of HMGB1
title_full_unstemmed Induction of acute lung inflammation in mice with hemorrhagic shock and resuscitation: role of HMGB1
title_short Induction of acute lung inflammation in mice with hemorrhagic shock and resuscitation: role of HMGB1
title_sort induction of acute lung inflammation in mice with hemorrhagic shock and resuscitation: role of hmgb1
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4193406/
https://www.ncbi.nlm.nih.gov/pubmed/25309129
http://dx.doi.org/10.1186/s12950-014-0030-7
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