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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...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Springer-Verlag
2010
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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. |
format | Online Article Text |
id | pubmed-3150797 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2010 |
publisher | Springer-Verlag |
record_format | MEDLINE/PubMed |
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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