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

Decreased plasma concentrations of apolipoprotein M in sepsis and systemic inflammatory response syndromes.
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DOI:
10.1186/cc11305
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发表时间:
2012-12-12
期刊:
Critical care (London, England)
影响因子:
--
通讯作者:
Dahlbäck B
Dahlbäck B
中科院分区:
其他
文献类型:
--
作者:
Kumaraswamy SB;Linder A;Åkesson P;Dahlbäck B

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载脂蛋白M(apoM)存在于血浆中5%的高密度脂蛋白(HDL)颗粒中。它是鞘氨醇-1-磷酸(S1 P)的载体,对血管屏障保护很重要。目的是确定脓毒症和全身炎症反应综合征(SIRS)期间apoM的血浆浓度,并将其与载脂蛋白A-I(apoA 1)、载脂蛋白B(apoB)、HDL-和低密度脂蛋白(LDL)-胆固醇水平相关联。分析来自以下患者的血浆样品:(1)严重脓毒症伴休克(n = 26);(2)严重脓毒症不伴休克(n = 44);(3)脓毒症(n = 100);(4)感染不伴SIRS(n = 43);和(5)SIRS不伴感染(n = 20)。采用酶联免疫吸附试验(ELISA)测定apoM、apoA 1和apoB的浓度。用商业HDL/LDL胆固醇测试测量总胆固醇、HDL-胆固醇和LDL-胆固醇浓度。ApoM浓度与急性期标志物呈负相关。因此,apoM表现为负急性期蛋白。在所有患者组中均观察到数值降低(P < 0.0001),在重症患者中观察到最剧烈的降低。ApoM水平与apoA 1、apoB、HDL和LDL胆固醇水平密切相关。与对照组相比,所有患者组的HDL和LDL胆固醇水平均较低(P < 0.0001),特别是HDL胆固醇。ApoA 1和apoB浓度仅在较严重的患者中较低。在脓毒症和SIRS期间,apoM的血浆浓度显著降低,降低的程度反映了疾病的严重程度。作为HDL屏障保护性S1 P的载体,apoM的减少可能有助于脓毒症和SIRS中观察到的血管渗漏增加。
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. 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. 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. 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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