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Systemic release of heat-shock protein 27 and 70 following severe trauma
Trauma represents a major cause of morbidity and mortality worldwide. The endogenous inflammatory response to trauma remains not fully elucidated. Pro-inflammation in the early phase is followed by immunosuppression leading to infections, multi-organ failure and mortality. Heat-shock proteins (HSPs)...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6610099/ https://www.ncbi.nlm.nih.gov/pubmed/31270381 http://dx.doi.org/10.1038/s41598-019-46034-w |
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author | Haider, Thomas Simader, Elisabeth Glück, Olaf Ankersmit, Hendrik J. Heinz, Thomas Hajdu, Stefan Negrin, Lukas L. |
author_facet | Haider, Thomas Simader, Elisabeth Glück, Olaf Ankersmit, Hendrik J. Heinz, Thomas Hajdu, Stefan Negrin, Lukas L. |
author_sort | Haider, Thomas |
collection | PubMed |
description | Trauma represents a major cause of morbidity and mortality worldwide. The endogenous inflammatory response to trauma remains not fully elucidated. Pro-inflammation in the early phase is followed by immunosuppression leading to infections, multi-organ failure and mortality. Heat-shock proteins (HSPs) act as intracellular chaperons but exert also extracellular functions. However, their role in acute trauma remains unknown. The aim of this study was to evaluate serum concentrations of HSP 27 and HSP 70 in severely injured patients. We included severely injured patients with an injury severity score of at least 16 and measured serum concentration of both markers at admission and on day two. We found significantly increased serum concentrations of both HSP 27 and HSP 70 in severely injured patients. Concomitant thoracic trauma lead to a further increase of both HSPs. Also, elevated concentrations of HSP 27 and HSP 70 were associated with poor outcome in these patients. Standard laboratory parameters did not correlate with neither HSP 27, nor with HSP 70. Our findings demonstrate involvement of systemic release of HSP 27 and HSP 70 after severe trauma and their potential as biomarker in polytraumatized patients. |
format | Online Article Text |
id | pubmed-6610099 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-66100992019-07-14 Systemic release of heat-shock protein 27 and 70 following severe trauma Haider, Thomas Simader, Elisabeth Glück, Olaf Ankersmit, Hendrik J. Heinz, Thomas Hajdu, Stefan Negrin, Lukas L. Sci Rep Article Trauma represents a major cause of morbidity and mortality worldwide. The endogenous inflammatory response to trauma remains not fully elucidated. Pro-inflammation in the early phase is followed by immunosuppression leading to infections, multi-organ failure and mortality. Heat-shock proteins (HSPs) act as intracellular chaperons but exert also extracellular functions. However, their role in acute trauma remains unknown. The aim of this study was to evaluate serum concentrations of HSP 27 and HSP 70 in severely injured patients. We included severely injured patients with an injury severity score of at least 16 and measured serum concentration of both markers at admission and on day two. We found significantly increased serum concentrations of both HSP 27 and HSP 70 in severely injured patients. Concomitant thoracic trauma lead to a further increase of both HSPs. Also, elevated concentrations of HSP 27 and HSP 70 were associated with poor outcome in these patients. Standard laboratory parameters did not correlate with neither HSP 27, nor with HSP 70. Our findings demonstrate involvement of systemic release of HSP 27 and HSP 70 after severe trauma and their potential as biomarker in polytraumatized patients. Nature Publishing Group UK 2019-07-03 /pmc/articles/PMC6610099/ /pubmed/31270381 http://dx.doi.org/10.1038/s41598-019-46034-w Text en © The Author(s) 2019 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Haider, Thomas Simader, Elisabeth Glück, Olaf Ankersmit, Hendrik J. Heinz, Thomas Hajdu, Stefan Negrin, Lukas L. Systemic release of heat-shock protein 27 and 70 following severe trauma |
title | Systemic release of heat-shock protein 27 and 70 following severe trauma |
title_full | Systemic release of heat-shock protein 27 and 70 following severe trauma |
title_fullStr | Systemic release of heat-shock protein 27 and 70 following severe trauma |
title_full_unstemmed | Systemic release of heat-shock protein 27 and 70 following severe trauma |
title_short | Systemic release of heat-shock protein 27 and 70 following severe trauma |
title_sort | systemic release of heat-shock protein 27 and 70 following severe trauma |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6610099/ https://www.ncbi.nlm.nih.gov/pubmed/31270381 http://dx.doi.org/10.1038/s41598-019-46034-w |
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