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Induced expression and functional effects of aquaporin-1 in human leukocytes in sepsis

INTRODUCTION: Gene expression profiling was performed via DNA microarrays in leukocytes from critically ill trauma patients nonseptic upon admission to the ICU, who subsequently developed either sepsis (n = 2) or severe sepsis and acute respiratory distress syndrome (n = 3). By comparing our results...

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Autores principales: Vassiliou, Alice G, Maniatis, Nikolaos A, Orfanos, Stylianos E, Mastora, Zafeiria, Jahaj, Edison, Paparountas, Triantafillos, Armaganidis, Apostolos, Roussos, Charis, Aidinis, Vassilis, Kotanidou, Anastasia
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2013
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Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4056620/
https://www.ncbi.nlm.nih.gov/pubmed/24028651
http://dx.doi.org/10.1186/cc12893
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author Vassiliou, Alice G
Maniatis, Nikolaos A
Orfanos, Stylianos E
Mastora, Zafeiria
Jahaj, Edison
Paparountas, Triantafillos
Armaganidis, Apostolos
Roussos, Charis
Aidinis, Vassilis
Kotanidou, Anastasia
author_facet Vassiliou, Alice G
Maniatis, Nikolaos A
Orfanos, Stylianos E
Mastora, Zafeiria
Jahaj, Edison
Paparountas, Triantafillos
Armaganidis, Apostolos
Roussos, Charis
Aidinis, Vassilis
Kotanidou, Anastasia
author_sort Vassiliou, Alice G
collection PubMed
description INTRODUCTION: Gene expression profiling was performed via DNA microarrays in leukocytes from critically ill trauma patients nonseptic upon admission to the ICU, who subsequently developed either sepsis (n = 2) or severe sepsis and acute respiratory distress syndrome (n = 3). By comparing our results with published expression profiling studies in animal models of sepsis and lung injury, we found aquaporin-1 to be differentially expressed across all studies. Our aim was to determine how the water channel aquaporin-1 is involved in regulating the immune response in critically ill patients during infection acquired in the ICU. METHODS: Following the results of the initial genetic screening study, we prospectively followed aquaporin-1 leukocyte expression patterns in patients with ICU-acquired sepsis who subsequently developed septic shock (n = 16) versus critically ill patients who were discharged without developing sepsis (n = 13). We additionally determined aquaporin-1 expression upon lipopolysaccharide (LPS) exposure and explored functional effects of aquaporin-1 induction in polymorphonuclear granulocytes (PMNs). RESULTS: Leukocyte aquaporin-1 expression was induced at the onset of sepsis (median 1.71-fold increase; interquartile range: 0.99 to 2.42, P = 0.012 from baseline) and was further increased upon septic shock (median 3.00-fold increase; interquartile range: 1.20 to 5.40, P = 0.023 from sepsis, Wilcoxon signed-rank test); no difference was observed between baseline and discharge in patients who did not develop sepsis. Stimulation of PMNs by LPS led to increased expression of aquaporin-1 in vitro, which could be abrogated by the NF-κB inhibitor EF-24. PMN hypotonic challenge resulted in a transient increase of the relative cell volume, which returned to baseline after 600 seconds, while incubation in the presence of LPS resulted in persistently increased cell volume. The latter could be abolished by blocking aquaporin-1 with mercury and restored by incubation in β-mercaptoethanol, which abrogated the action of mercury inhibition. CONCLUSIONS: Aquaporin-1 is induced in leukocytes of patients with ICU-acquired sepsis and exhibits higher expression in septic shock. This phenomenon may be due to LPS-triggered NF-κB activation that can also lead to alterations in plasma membrane permeability.
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spelling pubmed-40566202014-06-14 Induced expression and functional effects of aquaporin-1 in human leukocytes in sepsis Vassiliou, Alice G Maniatis, Nikolaos A Orfanos, Stylianos E Mastora, Zafeiria Jahaj, Edison Paparountas, Triantafillos Armaganidis, Apostolos Roussos, Charis Aidinis, Vassilis Kotanidou, Anastasia Crit Care Research INTRODUCTION: Gene expression profiling was performed via DNA microarrays in leukocytes from critically ill trauma patients nonseptic upon admission to the ICU, who subsequently developed either sepsis (n = 2) or severe sepsis and acute respiratory distress syndrome (n = 3). By comparing our results with published expression profiling studies in animal models of sepsis and lung injury, we found aquaporin-1 to be differentially expressed across all studies. Our aim was to determine how the water channel aquaporin-1 is involved in regulating the immune response in critically ill patients during infection acquired in the ICU. METHODS: Following the results of the initial genetic screening study, we prospectively followed aquaporin-1 leukocyte expression patterns in patients with ICU-acquired sepsis who subsequently developed septic shock (n = 16) versus critically ill patients who were discharged without developing sepsis (n = 13). We additionally determined aquaporin-1 expression upon lipopolysaccharide (LPS) exposure and explored functional effects of aquaporin-1 induction in polymorphonuclear granulocytes (PMNs). RESULTS: Leukocyte aquaporin-1 expression was induced at the onset of sepsis (median 1.71-fold increase; interquartile range: 0.99 to 2.42, P = 0.012 from baseline) and was further increased upon septic shock (median 3.00-fold increase; interquartile range: 1.20 to 5.40, P = 0.023 from sepsis, Wilcoxon signed-rank test); no difference was observed between baseline and discharge in patients who did not develop sepsis. Stimulation of PMNs by LPS led to increased expression of aquaporin-1 in vitro, which could be abrogated by the NF-κB inhibitor EF-24. PMN hypotonic challenge resulted in a transient increase of the relative cell volume, which returned to baseline after 600 seconds, while incubation in the presence of LPS resulted in persistently increased cell volume. The latter could be abolished by blocking aquaporin-1 with mercury and restored by incubation in β-mercaptoethanol, which abrogated the action of mercury inhibition. CONCLUSIONS: Aquaporin-1 is induced in leukocytes of patients with ICU-acquired sepsis and exhibits higher expression in septic shock. This phenomenon may be due to LPS-triggered NF-κB activation that can also lead to alterations in plasma membrane permeability. BioMed Central 2013 2013-09-12 /pmc/articles/PMC4056620/ /pubmed/24028651 http://dx.doi.org/10.1186/cc12893 Text en Copyright © 2013 Vassiliou et al.; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research
Vassiliou, Alice G
Maniatis, Nikolaos A
Orfanos, Stylianos E
Mastora, Zafeiria
Jahaj, Edison
Paparountas, Triantafillos
Armaganidis, Apostolos
Roussos, Charis
Aidinis, Vassilis
Kotanidou, Anastasia
Induced expression and functional effects of aquaporin-1 in human leukocytes in sepsis
title Induced expression and functional effects of aquaporin-1 in human leukocytes in sepsis
title_full Induced expression and functional effects of aquaporin-1 in human leukocytes in sepsis
title_fullStr Induced expression and functional effects of aquaporin-1 in human leukocytes in sepsis
title_full_unstemmed Induced expression and functional effects of aquaporin-1 in human leukocytes in sepsis
title_short Induced expression and functional effects of aquaporin-1 in human leukocytes in sepsis
title_sort induced expression and functional effects of aquaporin-1 in human leukocytes in sepsis
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4056620/
https://www.ncbi.nlm.nih.gov/pubmed/24028651
http://dx.doi.org/10.1186/cc12893
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