Plasma endotoxin level of healthy donors

Nádházi, Zoltán; Takáts, Annamária; Offenmüller, Katalin; Bertók, L

doi:10.1556/amicr.49.2002.1.15

Cited by 51 publications

(39 citation statements)

References 13 publications

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“…In that study it was shown that intragastrically applied 125 I-LPS, similarly prepared as the LPS in our present study, could be extracted in its entirety from the liver, thus showing that bioactive LPS is being absorbed from the gut and circulated through the body. Moreover, bioactive LPS is detectable in low amounts in the blood of healthy human subjects even in the apparent absence of infections (40,41), which would suggest that small amounts of LPS are being continuously absorbed from the gut, perhaps as part of a normal physiological process of yet unknown relevance.…”

Section: Discussionmentioning

confidence: 99%

Chylomicrons promote intestinal absorption of lipopolysaccharides

Ghoshal

Witta

Zhong

et al. 2009

Journal of Lipid Research

554

387

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Recent data suggest that dietary fat promotes intestinal absorption of lipopolysaccharides (LPS) from the gut microflora, which might contribute to various inflammatory disorders. The mechanism of fat-induced LPS absorption is unclear, however. Intestinal-epithelial cells can internalize LPS from the apical surface and transport LPS to the Golgi. The Golgi complex also contains newly formed chylomicrons, the lipoproteins that transport dietary longchain fat through mesenteric lymph and blood. Because LPS has affinity for chylomicrons, we hypothesized that chylomicron formation promotes LPS absorption. In agreement with our hypothesis, we found that CaCo-2 cells released more cell-associated LPS after incubation with oleic-acid (OA), a long-chain fatty acid that induces chylomicron formation, than with butyric acid (BA), a short-chain fatty acid that does not induce chylomicron formation. Moreover, the effect of OA was blocked by the inhibitor of chylomicron formation, Pluronic L-81. We also observed that intragastric triolein (TO) gavage was followed by increased plasma LPS, whereas gavage with tributyrin (TB), or TO plus Pluronic L-81, was not. Most intestinally absorbed LPS was present on chylomicron remnants (CM-R) in the blood. Chylomicron formation also promoted transport of LPS through mesenteric lymph nodes (MLN) and the production of TNFa mRNA in the MLN. Together, our data suggest that intestinal epithelial cells may release LPS on chylomicrons from cell-associated pools. Chylomicron-associated LPS may contribute to postprandial inflammatory responses or chronic diet-induced inflammation in chylomicron target tissues.-Ghoshal, S., J. Witta, J. Zhong, W. de Villiers, and E. Eckhardt. Chylomicrons promote intestinal absorption of lipopolysaccharides. J. Lipid Res. 2009. 50: 90-97.

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Section: Discussionmentioning

confidence: 99%

Chylomicrons promote intestinal absorption of lipopolysaccharides

Ghoshal

Witta

Zhong

et al. 2009

Journal of Lipid Research

554

387

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“…absorbed from the gut in healthy animals ( 12 ) and bioactived LPS is detectable in low amounts in the blood of healthy human subjects, even in the apparent absence of infections ( 21,22 ). Chylomicrons have been associated with metabolic endotoxemia.…”

Section: Discussionmentioning

confidence: 99%

Endotoxin increase after fat overload is related to postprandial hypertriglyceridemia in morbidly obese patients

Clemente‐Postigo

Queipo‐Ortuño

Murri

et al. 2012

Journal of Lipid Research

118

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Obesity is an increasingly prevalent health problem, very often accompanied by other diseases, the most common being insulin resistance, type 2 diabetes mellitus, and cardiovascular complications ( 1, 2 ). Furthermore, an association has been reported between obesity and both oxidative stress and increased infl ammation ( 3, 4 ). Obesity facilitates the development of a low-grade infl ammatory state, characterized by increased plasma levels of proinfl ammatory cytokines ( 4 ). However, the factors that trigger this low-grade infl ammation in obesity are unclear. Postprandial lipidemia has recently emerged as a potential candidate because the ingestion of a highfat meal leads to the systemic increase of a wide range of infl ammatory mediators ( 5-7 ) and an increase in oxidative stress markers ( 8 ). However, the cause of these postprandial events that occur in association with the postprandial triglyceride response remains poorly understood. A possible link is bacterial endotoxin [lipopolysaccharide (LPS)], a component of the Gram-negative bacteria cell wall that is present in large quantities in the human gut ( 9 ). Endotoxins circulate in the plasma Abstract The low-grade infl ammation observed in obesity has been associated with a high-fat diet, though this relation is not fully understood. Bacterial endotoxin, produced by gut microbiota, may be the linking factor. However, this has not been confi rmed in obese patients. To study the relationship between a high-fat diet and bacterial endotoxin, we analyzed postprandial endotoxemia in morbidly obese patients after a fat overload. The endotoxin levels were determined in serum and the chylomicron fraction at baseline and 3 h after a fat overload in 40 morbidly obese patients and their levels related with the degree of insulin resistance and postprandial hypertriglyceridemia. The morbidly obese patients with the highest postprandial hypertriglyceridemia showed a signifi cant increase in lipopolysaccharide (LPS) levels in serum and the chylomicron fraction after the fat overload. Postprandial chylomicron LPS levels correlated positively with the di ff erence between postprandial triglycerides and baseline triglycerides. There were no signifi cant correlations between C-reactive protein (CRP) and LPS levels. The main variables contributing to serum LPS levels after fat overload were baseline and postprandial triglyceride levels but not glucose or insulin resistance. Additionally, superoxide dismutase activity decreased signifi cantly after the fat overload. Postprandial LPS increase after a fat overload is related to postprandial hypertriglyceridemia but not to degree of insulin resistance in morbidly obese patients. -Clemente-Postigo, M., M. I. Queipo-Ortuño,

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“…For recognition of the LPS molecular structure by the hosts, conserved ‘microorganism-associated molecular pattern'- or ‘pathogen-associated molecular pattern'-specific elements have been selected during evolution [35,36]. Derived from the gut Gram-negative bacteria, endotoxin continuously enters the blood in a ‘physiological manner' through the intestinal epithelial cells and the vessels of vena portae, resulting in measurable plasma levels in every healthy human subject, ranging from 0.01 to 1.0 endotoxin units/ml [37,38]. …”

Section: Bacterial Lps/bacterial Endotoxinmentioning

confidence: 99%

The Immunomodulatory Role of Bile Acids

Sipka

Bruckner

2014

Int Arch Allergy Immunol

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Enzymatic oxidation of cholesterol generates numerous distinct bile acids which function both as detergents that facilitate the digestion and absorption of dietary lipids and as hormones that activate five distinct receptors. Activation of these receptors alters gene expression in multiple tissues, leading to changes not only in bile acid metabolism but also in glucose homeostasis, lipid and lipoprotein metabolism, energy expenditure, intestinal motility, bacterial growth, inflammation, and in the liver-gut axis. This review focuses on the present knowledge regarding the physiologic and pathologic role of bile acids and their immunomodulatory role, with particular attention to bacterial lipopolysaccharides (endotoxins) and bile acid and immunological disorders. The specific role that bile acids play in the regulation of innate immunity, various systemic inflammations, inflammatory bowel diseases, allergy, psoriasis, cholestasis, obesity, metabolic syndrome, alcoholic liver disease, and colon cancer will be reviewed.

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Plasma endotoxin level of healthy donors

Cited by 51 publications

References 13 publications

Chylomicrons promote intestinal absorption of lipopolysaccharides

Chylomicrons promote intestinal absorption of lipopolysaccharides

Endotoxin increase after fat overload is related to postprandial hypertriglyceridemia in morbidly obese patients

The Immunomodulatory Role of Bile Acids

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