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Isolated blunt chest injury leads to transient activation of circulating neutrophils

INTRODUCTION: The acute respiratory distress syndrome (ARDS) is a severe and frequently seen complication in multi-trauma patients. ARDS is caused by an excessive innate immune response with a clear role for neutrophils. As ARDS is more frequently seen in trauma patients with chest injury, we invest...

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Autores principales: Visser, T., Hietbrink, F., Groeneveld, K. M., Koenderman, L., Leenen, L. P. H.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer-Verlag 2010
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3150797/
https://www.ncbi.nlm.nih.gov/pubmed/21837259
http://dx.doi.org/10.1007/s00068-010-0041-x
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author Visser, T.
Hietbrink, F.
Groeneveld, K. M.
Koenderman, L.
Leenen, L. P. H.
author_facet Visser, T.
Hietbrink, F.
Groeneveld, K. M.
Koenderman, L.
Leenen, L. P. H.
author_sort Visser, T.
collection PubMed
description INTRODUCTION: The acute respiratory distress syndrome (ARDS) is a severe and frequently seen complication in multi-trauma patients. ARDS is caused by an excessive innate immune response with a clear role for neutrophils. As ARDS is more frequently seen in trauma patients with chest injury, we investigated the influence of chest injury on the systemic neutrophil response and the development of ARDS. MATERIALS AND METHODS: Thirteen patients with isolated blunt chest injury [abbreviated injury score (AIS) 2–5] were included. To avoid systemic inflammation caused by tissue damage outside the thorax, injuries to other regions than the chest did not exceed an AIS of 2. At 3, 9 and 24 h after injury, the expression of circulating activating molecules on neutrophils and levels of circulating interleukine (IL)-6 were determined. Blood samples from eight healthy volunteers were used as control. RESULTS: Blunt chest injury resulted in the activation of circulating neutrophils, as characterized by a decreased expression of l-selectin (CD62L), CXCR2 (CD182b) and C5aR (CD88) compared to control (p < 0.05). Expression of l-selectin, CXCR2 and C5aR was partially restored at 24 h after injury. In addition, the mean expression of FcγRIII (CD16) dropped (p < 0.001), indicating the recruitment of young neutrophils into the circulation. IL-6 levels increased to a maximum mean concentration of 86 ± 31 pg/ml at 24 h postinjury. None of the patients developed ARDS. CONCLUSION: Blunt chest trauma caused a systemic inflammatory reaction with transient activation of neutrophils and mobilization of young neutrophils into the circulation. Isolated chest injury, however, was not abundant enough to cause ARDS, so a second hit appears crucial.
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spelling pubmed-31507972011-08-09 Isolated blunt chest injury leads to transient activation of circulating neutrophils Visser, T. Hietbrink, F. Groeneveld, K. M. Koenderman, L. Leenen, L. P. H. Eur J Trauma Emerg Surg Original Article INTRODUCTION: The acute respiratory distress syndrome (ARDS) is a severe and frequently seen complication in multi-trauma patients. ARDS is caused by an excessive innate immune response with a clear role for neutrophils. As ARDS is more frequently seen in trauma patients with chest injury, we investigated the influence of chest injury on the systemic neutrophil response and the development of ARDS. MATERIALS AND METHODS: Thirteen patients with isolated blunt chest injury [abbreviated injury score (AIS) 2–5] were included. To avoid systemic inflammation caused by tissue damage outside the thorax, injuries to other regions than the chest did not exceed an AIS of 2. At 3, 9 and 24 h after injury, the expression of circulating activating molecules on neutrophils and levels of circulating interleukine (IL)-6 were determined. Blood samples from eight healthy volunteers were used as control. RESULTS: Blunt chest injury resulted in the activation of circulating neutrophils, as characterized by a decreased expression of l-selectin (CD62L), CXCR2 (CD182b) and C5aR (CD88) compared to control (p < 0.05). Expression of l-selectin, CXCR2 and C5aR was partially restored at 24 h after injury. In addition, the mean expression of FcγRIII (CD16) dropped (p < 0.001), indicating the recruitment of young neutrophils into the circulation. IL-6 levels increased to a maximum mean concentration of 86 ± 31 pg/ml at 24 h postinjury. None of the patients developed ARDS. CONCLUSION: Blunt chest trauma caused a systemic inflammatory reaction with transient activation of neutrophils and mobilization of young neutrophils into the circulation. Isolated chest injury, however, was not abundant enough to cause ARDS, so a second hit appears crucial. Springer-Verlag 2010-07-27 2011 /pmc/articles/PMC3150797/ /pubmed/21837259 http://dx.doi.org/10.1007/s00068-010-0041-x Text en © The Author(s) 2010 https://creativecommons.org/licenses/by-nc/4.0/ This article is distributed under the terms of the Creative Commons Attribution Noncommercial License which permits any noncommercial use, distribution, and reproduction in any medium, provided the original author(s) and source are credited.
spellingShingle Original Article
Visser, T.
Hietbrink, F.
Groeneveld, K. M.
Koenderman, L.
Leenen, L. P. H.
Isolated blunt chest injury leads to transient activation of circulating neutrophils
title Isolated blunt chest injury leads to transient activation of circulating neutrophils
title_full Isolated blunt chest injury leads to transient activation of circulating neutrophils
title_fullStr Isolated blunt chest injury leads to transient activation of circulating neutrophils
title_full_unstemmed Isolated blunt chest injury leads to transient activation of circulating neutrophils
title_short Isolated blunt chest injury leads to transient activation of circulating neutrophils
title_sort isolated blunt chest injury leads to transient activation of circulating neutrophils
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3150797/
https://www.ncbi.nlm.nih.gov/pubmed/21837259
http://dx.doi.org/10.1007/s00068-010-0041-x
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