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Inflammation-associated changes in lipid composition and the organization of the erythrocyte membrane

BACKGROUND: Reduced erythrocyte survival and deformability may contribute to the so-called anemia of inflammation observed in septic patients. Erythrocyte structure and function are affected by both the membrane lipid composition and the organization. We therefore aimed to determine whether these pa...

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Autores principales: Dinkla, Sip, van Eijk, Lucas T., Fuchs, Beate, Schiller, Jürgen, Joosten, Irma, Brock, Roland, Pickkers, Peter, Bosman, Giel J.C.G.M.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4864322/
https://www.ncbi.nlm.nih.gov/pubmed/27200268
http://dx.doi.org/10.1016/j.bbacli.2016.03.007
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author Dinkla, Sip
van Eijk, Lucas T.
Fuchs, Beate
Schiller, Jürgen
Joosten, Irma
Brock, Roland
Pickkers, Peter
Bosman, Giel J.C.G.M.
author_facet Dinkla, Sip
van Eijk, Lucas T.
Fuchs, Beate
Schiller, Jürgen
Joosten, Irma
Brock, Roland
Pickkers, Peter
Bosman, Giel J.C.G.M.
author_sort Dinkla, Sip
collection PubMed
description BACKGROUND: Reduced erythrocyte survival and deformability may contribute to the so-called anemia of inflammation observed in septic patients. Erythrocyte structure and function are affected by both the membrane lipid composition and the organization. We therefore aimed to determine whether these parameters are affected during systemic inflammation. METHODS: A sensitive matrix-assisted laser desorption and ionization time-of-flight mass spectrometric method was used to investigate the effect of plasma components of 10 patients with septic shock and of 10 healthy volunteers subjected to experimental endotoxemia on erythrocyte membrane lipid composition. RESULTS: Incubation of erythrocytes from healthy control donors with plasma from patients with septic shock resulted in membrane phosphatidylcholine hydrolysis into lysophosphatidylcholine (LPC). Plasma from volunteers undergoing experimental human endotoxemia did not induce LPC formation. The secretory phospholipase A(2) IIA concentration was enhanced up to 200-fold in plasma of septic patients and plasma from endotoxin-treated subjects, but did not correlate with the ability of these plasmas to generate LPC. Erythrocyte phosphatidylserine exposure increased up to two-fold during experimental endotoxemia. CONCLUSIONS: Erythrocyte membrane lipid remodeling as reflected by LPC formation and/or PS exposure occurs during systemic inflammation in a secretory phospholipase A(2) IIA-independent manner. GENERAL SIGNIFICANCE: Sepsis-associated inflammation induces a lipid remodeling of the erythrocyte membrane that is likely to affect erythrocyte function and survival, and that is not fully mimicked by experimental endotoxemia.
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spelling pubmed-48643222016-05-19 Inflammation-associated changes in lipid composition and the organization of the erythrocyte membrane Dinkla, Sip van Eijk, Lucas T. Fuchs, Beate Schiller, Jürgen Joosten, Irma Brock, Roland Pickkers, Peter Bosman, Giel J.C.G.M. BBA Clin Regular Article BACKGROUND: Reduced erythrocyte survival and deformability may contribute to the so-called anemia of inflammation observed in septic patients. Erythrocyte structure and function are affected by both the membrane lipid composition and the organization. We therefore aimed to determine whether these parameters are affected during systemic inflammation. METHODS: A sensitive matrix-assisted laser desorption and ionization time-of-flight mass spectrometric method was used to investigate the effect of plasma components of 10 patients with septic shock and of 10 healthy volunteers subjected to experimental endotoxemia on erythrocyte membrane lipid composition. RESULTS: Incubation of erythrocytes from healthy control donors with plasma from patients with septic shock resulted in membrane phosphatidylcholine hydrolysis into lysophosphatidylcholine (LPC). Plasma from volunteers undergoing experimental human endotoxemia did not induce LPC formation. The secretory phospholipase A(2) IIA concentration was enhanced up to 200-fold in plasma of septic patients and plasma from endotoxin-treated subjects, but did not correlate with the ability of these plasmas to generate LPC. Erythrocyte phosphatidylserine exposure increased up to two-fold during experimental endotoxemia. CONCLUSIONS: Erythrocyte membrane lipid remodeling as reflected by LPC formation and/or PS exposure occurs during systemic inflammation in a secretory phospholipase A(2) IIA-independent manner. GENERAL SIGNIFICANCE: Sepsis-associated inflammation induces a lipid remodeling of the erythrocyte membrane that is likely to affect erythrocyte function and survival, and that is not fully mimicked by experimental endotoxemia. Elsevier 2016-04-03 /pmc/articles/PMC4864322/ /pubmed/27200268 http://dx.doi.org/10.1016/j.bbacli.2016.03.007 Text en © 2016 The Authors http://creativecommons.org/licenses/by/4.0/ This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Regular Article
Dinkla, Sip
van Eijk, Lucas T.
Fuchs, Beate
Schiller, Jürgen
Joosten, Irma
Brock, Roland
Pickkers, Peter
Bosman, Giel J.C.G.M.
Inflammation-associated changes in lipid composition and the organization of the erythrocyte membrane
title Inflammation-associated changes in lipid composition and the organization of the erythrocyte membrane
title_full Inflammation-associated changes in lipid composition and the organization of the erythrocyte membrane
title_fullStr Inflammation-associated changes in lipid composition and the organization of the erythrocyte membrane
title_full_unstemmed Inflammation-associated changes in lipid composition and the organization of the erythrocyte membrane
title_short Inflammation-associated changes in lipid composition and the organization of the erythrocyte membrane
title_sort inflammation-associated changes in lipid composition and the organization of the erythrocyte membrane
topic Regular Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4864322/
https://www.ncbi.nlm.nih.gov/pubmed/27200268
http://dx.doi.org/10.1016/j.bbacli.2016.03.007
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