Effect of Plasma Phospholipid Transfer Protein Deficiency on Lethal Endotoxemia in Mice

Gautier, Thomas; Klein, Alexis; Deckert, Valérie; Desrumaux, Catherine; Ogier, Nicolas; Sberna, Anne-Laure; Paul, Catherine; Guern, Naïg Le; Athias, Anne; Montange, Thomas; Monier, Serge; Piard, F; Jiang, Xian‐Cheng; Masson, David; Lagrost, Laurent

doi:10.1074/jbc.m802802200

Cited by 62 publications

(96 citation statements)

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“…The combination of the LAL and HPLC/ MS/MS analyses in the present study provided new evidence of the intrinsic capacity of plasma to neutralize the activity of LPS. Alteration of the LAL to HPLC/MS/MS ratio may to a large extent be due to the recognized ability of endogenous plasma lipoproteins to bind and neutralize LPS, because signifi cantly lower values were calculated in wild-type mice than in PLTP-defi cient mice, which are known to have a weaker ability to associate LPS with lipoproteins and to neutralize its biological activity ( 14 ). Here, rather than a surrogate for quantitation of total LPS amounts, the LAL assay was used as a direct in vivo evaluation of biologically active LPS.…”

Section: Discussionmentioning

confidence: 99%

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Quantitative lipopolysaccharide analysis using HPLC/MS/MS and its combination with the limulus amebocyte lysate assay

Barros

Gautier

Sali

et al. 2015

Journal of Lipid Research

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109

103

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Systemic infl ammatory response syndrome (SIRS) is defi ned by a cluster of clinical signs that include tachycardia, leukocytosis, tachypnoea, and pyrexia ( 1 ). Although SIRS is a major consequence of sepsis (i.e., a deleterious, nonresolving infl ammatory response to infection that can lead to multiple organ dysfunction and septic shock), it can be caused by many pathological events that are not associated with the bacterial infection ( 1 ). It is of major importance to distinguish between noninfectious SIRS, sepsis, and septic shock in critically ill patients because these groups of patients are markedly different in terms of care and clinical outcome. Positive microbiological identifi cation tests [using conventional microbiological tests or bacterial DNA detection ( 2 ) as well as a number of infl ammatory and infectious biomarkers, including cytokines, procalcitonin, immune cell markers or a combination of these ( 3 )] have been proposed, but at this stage, none has proved to be reliable enough to ascertain the occurrence and extent of infection in high-risk patients with SIRS. Interestingly, and as documented further by our group in the prospective multicenter cohort EPISS study ( 4 ), Gramnegative bacilli are the most frequently identifi ed pathogens in patients with septic shock. In this context, the direct quantitation of the culprit component of the Gram-negative bacterium [i.e., lipopolysaccharide (LPS), which triggers SIRS by interacting with the CD14/Toll-like receptor 4 /myeloid differentiation factor 2 receptor complex at the surface of leukocytes ( 1 ) Abbreviations: 3HM, 3-hydroxymyristic acid or 3-hydroxymyristate; LAL, limulus amebocyte lysate; LOD, limit of detection; LOQ, limit of quantifi cation; LPS, lipopolysaccharide; PLTP, phospholipid transfer protein; SIRS, systemic infl ammatory response syndrome; SOFA, sequential organ failure assessment .

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Section: Discussionmentioning

confidence: 99%

“…Silylating solution was then evaporated under an N 2 stream. Finally, 100 µl of hexane was added, and 1 µl of the mixture was injected in the split/splitless mode (split ratio 10:1) as previously described ( 14 ) on an Agilent GC 6890, MSD 5973 device.…”

Section: Gc/ms Analysismentioning

confidence: 99%

Quantitative lipopolysaccharide analysis using HPLC/MS/MS and its combination with the limulus amebocyte lysate assay

Barros

Gautier

Sali

et al. 2015

Journal of Lipid Research

Self Cite

109

103

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“…Although it is promising, the PLTP inhibition strategy should be considered with caution because the inhibition of PLTP activity might at the same time modify the formation of protein complexes implicated in host defenses 5 and slow down lipopolysaccharide detoxification. 12 …”

Section: Discussionmentioning

confidence: 99%

“…5 In support of this view, PLTP expression in the mouse was found to increase the production of apoB-containing lipoproteins by the liver 6 and intestine, 7 to decrease very low density lipoprotein (VLDL) catabolism, 8 to reduce the antioxidant protection of atherogenic lipoproteins, 9,10 to trigger inflammation, 11 and to promote the association of lipopolysaccharides with circulating lipoproteins. 12 All these properties have long been shown to influence the atherosclerotic process, whether acting individually or in a combined manner.…”

mentioning

confidence: 99%

Worsening of Diet-Induced Atherosclerosis in a New Model of Transgenic Rabbit Expressing the Human Plasma Phospholipid Transfer Protein

Masson

Deckert

Gautier

et al. 2011

ATVB

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Objective-Plasma phospholipid transfer protein (PLTP) is involved in intravascular lipoprotein metabolism. PLTP is known to act through 2 main mechanisms: by remodeling high-density lipoproteins (HDL) and by increasing apolipoprotein (apo) B-containing lipoproteins. The aim of this study was to generate a new model of human PLTP transgenic (HuPLTPTg) rabbit and to determine whether PLTP expression modulates atherosclerosis in this species that, unlike humans and mice, displays naturally very low PLTP activity. Methods and Results-In HuPLTPTg rabbits, the human PLTP cDNA was placed under the control of the human eF1-␣ gene promoter, resulting in a widespread tissue expression pattern and in increased plasma PLTP. The HuPLTPTg rabbits showed a significant increase in the cholesterol content of the plasma apoB-containing lipoprotein fractions, with a more severe trait when animals were fed a cholesterol-rich diet. In contrast, HDL cholesterol level was not modified in HuPLTPTg rabbits. Formation of aortic fatty streaks was increased in hypercholesterolemic HuPLTPTg animals as compared with nontransgenic littermates. Key Words: atherosclerosis Ⅲ lipoproteins Ⅲ metabolism Ⅲ transgenic models H uman plasma contains 2 distinct lipid transfer proteins (cholesteryl ester transfer protein [CETP] and phospholipid transfer protein [PLTP]) that promote the rapid exchange of lipid species between circulating lipoproteins, as well as between circulating lipoproteins and cells. 1 Although most reported data agree that the putative implication of CETP in lipoprotein metabolism and atherosclerotic process mostly concerns the net transfer of cholesteryl esters from antiatherogenic high-density lipoproteins (HDL) to potentially atherogenic apolipoprotein (apo) B-containing lipoproteins, 1 the precise function of PLTP and its consequences in terms of atherogenesis remain a matter of debate. PLTP was identified initially for its ability to promote the transfer of phospholipids from triglyceride-rich lipoproteins to HDL in the postprandial phase. 2 Subsequent studies reported that PLTP is also a key player in the HDL conversion process, leading to the emergence of large and small HDL products. 3,4 Recently, PLTP in human plasma was shown to reside mainly on lipid-poor complexes in association with proteins linked to immunity and inflammation, suggesting that the biological function of PLTP is rather complex in nature. 5 In support of this view, PLTP expression in the mouse was found to increase the production of apoB-containing lipoproteins by the liver 6 and intestine, 7 to decrease very low density lipoprotein (VLDL) catabolism, 8 to reduce the antioxidant protection of atherogenic lipoproteins, 9,10 to trigger inflammation, 11 and to promote the association of lipopolysaccharides with circulating lipoproteins. 12 All these properties have long been shown to influence the atherosclerotic process, whether acting individually or in a combined manner. Conclusion-HumanHigh plasma PLTP concentrations were earlier reported in diabetic...

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“…This neutralization results from the link of lipoproteins to their receptors notably in the liver, inducing LPS clearance with bile secretion (Eichbaum et al, 1991;Harris et al, 1993Harris et al, , 1998Vreugdenhil et al, 2003). Not only LBP but also the phospholipid transfer protein (PLTP) can bind LPS and contribute to detoxification during septic shocks (Gautier et al, 2008). Vors et al (2014).…”

Section: Endotoxins Are Proinflammatory Moleculesmentioning

confidence: 99%

Dietary lipid emulsions and endotoxemia

Michalski¹,

Vors²,

Lecomte³

et al. 2016

OCL

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-The low-grade inflammation observed in obesity is a risk factor for cardiovascular diseases and insulin resistance. Among factors triggering such inflammation, recent works revealed the role of bacterial lipopolysaccharides (LPS), so-called endotoxins. LPS are naturally present in the gut via the intestinal microbiota. Recent studies show that they can induce in plasma a metabolic endotoxemia after the consumption of unbalanced hyperlipidic meals. This article reviews recent knowledge gained on the role of intestinal lipid absorption and the composition of dietary lipids on: (i) the induction of metabolic endotoxemia, (ii) the types of plasma transporters of LPS and (iii) associated low-grade inflammation. Notably, lipids are present in foods under various physicochemical structures and notably in emulsified form. Our recent works reveal that such structure and the type of emulsifier can modulate postprandial lipemia; recent results on the possible consequences on metabolic endotoxemia will be discussed.Keywords: Nutrition / fat / oil / emulsifier / inflammation Résumé -Émulsions lipidiques alimentaires et endotoxémie. L'inflammation à bas bruit observée en situation d'obésité représente un facteur de risque cardiovasculaire et d'insulinorésistance. Parmi les facteurs responsables de cette inflammation, des travaux récents ont révélé l'implication des lipopolysaccharides bactériens, aussi appelés endotoxines. Ces endotoxines sont naturellement présentes dans le tractus digestif via le microbiote intestinal. Des études récentes montrent qu'elles peuvent générer une endotoxémie métabolique dans le plasma suite à la consommation de repas déséquilibrés hyperlipidiques. L'objectif de cette revue est de faire le point sur les connaissances récentes concernant le rôle de l'absorption intestinale des lipides et de la composition de ces derniers sur : (i) l'établissement d'une endotoxémie métabolique, (ii) la qualité des transporteurs plasmatiques des LPS et (iii) l'inflammation à bas bruit associée. En particulier, les lipides sont présents dans les aliments sous différentes structures physico-chimiques et notamment sous forme émulsionnée. Nos travaux récents montrent que cette structure est à même de moduler la lipémie postprandiale. Des résultats récents sur les possibles conséquences sur l'endotoxémie métabolique sont discutés.

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Effect of Plasma Phospholipid Transfer Protein Deficiency on Lethal Endotoxemia in Mice

Cited by 62 publications

References 61 publications

Quantitative lipopolysaccharide analysis using HPLC/MS/MS and its combination with the limulus amebocyte lysate assay

Quantitative lipopolysaccharide analysis using HPLC/MS/MS and its combination with the limulus amebocyte lysate assay

Worsening of Diet-Induced Atherosclerosis in a New Model of Transgenic Rabbit Expressing the Human Plasma Phospholipid Transfer Protein

Dietary lipid emulsions and endotoxemia

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