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Decreased plasma concentrations of apolipoprotein M in sepsis and systemic inflammatory response syndromes

INTRODUCTION: Apolipoprotein M (apoM) is present in 5% of high-density lipoprotein (HDL) particles in plasma. It is a carrier of sphingosine-1-phosphate (S1P), which is important for vascular barrier protection. The aim was to determine the plasma concentrations of apoM during sepsis and systemic in...

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Autores principales: Kumaraswamy, Sunil B, Linder, Adam, Åkesson, Per, Dahlbäck, Björn
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3681389/
https://www.ncbi.nlm.nih.gov/pubmed/22512779
http://dx.doi.org/10.1186/cc11305
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author Kumaraswamy, Sunil B
Linder, Adam
Åkesson, Per
Dahlbäck, Björn
author_facet Kumaraswamy, Sunil B
Linder, Adam
Åkesson, Per
Dahlbäck, Björn
author_sort Kumaraswamy, Sunil B
collection PubMed
description INTRODUCTION: Apolipoprotein M (apoM) is present in 5% of high-density lipoprotein (HDL) particles in plasma. It is a carrier of sphingosine-1-phosphate (S1P), which is important for vascular barrier protection. The aim was to determine the plasma concentrations of apoM during sepsis and systemic inflammatory response syndrome (SIRS) and correlate them to levels of apolipoprotein A-I (apoA1), apolipoprotein B (apoB), HDL-, and low-density lipoprotein (LDL)-cholesterol. METHODS: Plasma samples from patients with (1), severe sepsis with shock (n = 26); (2), severe sepsis without shock (n = 44); (3), sepsis (n = 100); (4), infections without SIRS (n = 43); and (5) SIRS without infection (n = 20) were analyzed. The concentrations of apoM, apoA1, and apoB were measured with enzyme-linked immunosorbent assays (ELISAs). Total, HDL-, and LDL-cholesterol concentrations were measured with a commercial HDL/LDL cholesterol test. RESULTS: ApoM concentrations correlated negatively to acute-phase markers. Thus, apoM behaved as a negative acute-phase protein. Decreased values were observed in all patient groups (P < 0.0001), with the most drastic decreases observed in the severely sick patients. ApoM levels correlated strongly to those of apoA1, apoB, HDL, and LDL cholesterol. The HDL and LDL cholesterol levels were low in all patient groups, as compared with controls (P < 0.0001), in particular, HDL cholesterol. ApoA1 and apoB concentrations were low only in the more severely affected patients. CONCLUSIONS: During sepsis and SIRS, the plasma concentrations of apoM decrease dramatically, the degree of decrease reflecting the severity of the disease. As a carrier for barrier-protective S1P in HDL, the decrease in apoM could contribute to the increased vascular leakage observed in sepsis and SIRS.
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spelling pubmed-36813892013-06-25 Decreased plasma concentrations of apolipoprotein M in sepsis and systemic inflammatory response syndromes Kumaraswamy, Sunil B Linder, Adam Åkesson, Per Dahlbäck, Björn Crit Care Research INTRODUCTION: Apolipoprotein M (apoM) is present in 5% of high-density lipoprotein (HDL) particles in plasma. It is a carrier of sphingosine-1-phosphate (S1P), which is important for vascular barrier protection. The aim was to determine the plasma concentrations of apoM during sepsis and systemic inflammatory response syndrome (SIRS) and correlate them to levels of apolipoprotein A-I (apoA1), apolipoprotein B (apoB), HDL-, and low-density lipoprotein (LDL)-cholesterol. METHODS: Plasma samples from patients with (1), severe sepsis with shock (n = 26); (2), severe sepsis without shock (n = 44); (3), sepsis (n = 100); (4), infections without SIRS (n = 43); and (5) SIRS without infection (n = 20) were analyzed. The concentrations of apoM, apoA1, and apoB were measured with enzyme-linked immunosorbent assays (ELISAs). Total, HDL-, and LDL-cholesterol concentrations were measured with a commercial HDL/LDL cholesterol test. RESULTS: ApoM concentrations correlated negatively to acute-phase markers. Thus, apoM behaved as a negative acute-phase protein. Decreased values were observed in all patient groups (P < 0.0001), with the most drastic decreases observed in the severely sick patients. ApoM levels correlated strongly to those of apoA1, apoB, HDL, and LDL cholesterol. The HDL and LDL cholesterol levels were low in all patient groups, as compared with controls (P < 0.0001), in particular, HDL cholesterol. ApoA1 and apoB concentrations were low only in the more severely affected patients. CONCLUSIONS: During sepsis and SIRS, the plasma concentrations of apoM decrease dramatically, the degree of decrease reflecting the severity of the disease. As a carrier for barrier-protective S1P in HDL, the decrease in apoM could contribute to the increased vascular leakage observed in sepsis and SIRS. BioMed Central 2012 2012-04-18 /pmc/articles/PMC3681389/ /pubmed/22512779 http://dx.doi.org/10.1186/cc11305 Text en Copyright ©2012 Dahlback 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
Kumaraswamy, Sunil B
Linder, Adam
Åkesson, Per
Dahlbäck, Björn
Decreased plasma concentrations of apolipoprotein M in sepsis and systemic inflammatory response syndromes
title Decreased plasma concentrations of apolipoprotein M in sepsis and systemic inflammatory response syndromes
title_full Decreased plasma concentrations of apolipoprotein M in sepsis and systemic inflammatory response syndromes
title_fullStr Decreased plasma concentrations of apolipoprotein M in sepsis and systemic inflammatory response syndromes
title_full_unstemmed Decreased plasma concentrations of apolipoprotein M in sepsis and systemic inflammatory response syndromes
title_short Decreased plasma concentrations of apolipoprotein M in sepsis and systemic inflammatory response syndromes
title_sort decreased plasma concentrations of apolipoprotein m in sepsis and systemic inflammatory response syndromes
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3681389/
https://www.ncbi.nlm.nih.gov/pubmed/22512779
http://dx.doi.org/10.1186/cc11305
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