Endotoxin release and endotoxin neutralizing capacity during colonoscopy

Bölke, Edwin; Jehle, Peter; Storck, M.; Nothnagel, B.; Stănescu, Anca Daniela; Orth, Klaus

doi:10.1016/s0009-8981(00)00373-9

Cited by 18 publications

(17 citation statements)

References 17 publications

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“…To our knowledge, this is the first time that these observations have been made in human subjects, although increased plasma endotoxin exposure, as measured both directly and by ENC, has been observed after colonoscopy (12), major surgery (20), extreme physical exertion (27), and acute exposure to large amounts of alcohol (which disrupts intestinal barrier function) (20,28). Thus, the notion of endotoxin release from the gut into All values are x Ȁ SEM; n ҃ 12.…”

Section: Discussionmentioning

confidence: 80%

“…Numerous studies have shown that these substances are depleted after endotoxin exposure (12,20,21). Thus, measurement of ENC of the plasma samples may show prior exposure to endotoxin, which would be invisible to intermittent monitoring.…”

Section: Endotoxin Neutralization Capacity Assaysmentioning

confidence: 99%

“…For this reason, we aimed to validate the results of the direct LAL assays by using a more robust measure of prior endotoxin exposure, the ENC assay (12,20,21). Overall, recovered endotoxin increased on average 18% after the high-fat meal and 12% after the high-fat meal with cigarettes (P 0.05 for both), which indicates a significant reduction in ENC (Figure 2).…”

Section: Measurements Of Endotoxin Neutralization Capacitymentioning

confidence: 99%

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A high-fat meal induces low-grade endotoxemia: evidence of a novel mechanism of postprandial inflammation

Erridge

Attinà

Spickett

et al. 2007

The American Journal of Clinical Nutrition

651

466

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Background: Bacterial endotoxin is a potently inflammatory antigen that is abundant in the human gut. Endotoxin circulates at low concentrations in the blood of all healthy individuals, although elevated concentrations are associated with an increased risk of atherosclerosis. Objective: We sought to determine whether a high-fat meal or smoking increases plasma endotoxin concentrations and whether such concentrations are of physiologic relevance. Design: Plasma endotoxin and endotoxin neutralization capacity were measured for 4 h in 12 healthy men after no meal, 3 cigarettes, a high-fat meal, or a high-fat meal with 3 cigarettes by using the limulus assay. Results: Baseline endotoxin concentrations were 8.2 pg/mL (interquartile range: 3.4 -13.5 pg/mL) but increased significantly (P 0.05) by Ȃ50% after a high-fat meal or after a high-fat meal with cigarettes but not after no meal or cigarettes alone. These results were validated by the observations that a high-fat meal with or without cigarettes, but not no meal or smoking, also significantly (P 0.05) reduced plasma endotoxin neutralization capacity, which is an indirect measure of endotoxin exposure. Human monocytes, but not aortic endothelial cells, were responsive to transient (30 s) or lowdose (10 pg/mL) exposure to endotoxin. However, plasma from whole blood treated with as little as 10 pg endotoxin/mL increased the endothelial cell expression of E-selectin, at least partly via tumor necrosis factor-␣-induced cellular activation. Conclusions: Low-grade endotoxemia may contribute to the postprandial inflammatory state and could represent a novel potential contributor to endothelial activation and the development of atherosclerosis.Am J Clin Nutr 2007;86:1286 -92.

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Section: Discussionmentioning

confidence: 80%

Section: Endotoxin Neutralization Capacity Assaysmentioning

confidence: 99%

Section: Measurements Of Endotoxin Neutralization Capacitymentioning

confidence: 99%

See 1 more Smart Citation

A high-fat meal induces low-grade endotoxemia: evidence of a novel mechanism of postprandial inflammation

Erridge

Attinà

Spickett

et al. 2007

The American Journal of Clinical Nutrition

651

466

View full text Add to dashboard Cite

show abstract

“…Depending on individuals and according to innate immunity, many compounds can participate in neutralizing or enhancing endotoxin activity in plasma. Therefore, several authors aimed to use more robust markers of plasma endotoxin exposure than only LPS measurements by LAL assay [12,[23][24][25]. In human plasma, we therefore measured the soluble form of the receptor cluster of differentiation 14 (sCD14) [26,27], which is induced during septic diseases [28] and can also be considered as a marker of endotoxin in plasma [29][30][31].…”

Section: Scd14 Assaymentioning

confidence: 99%

Emulsified lipids increase endotoxemia: possible role in early postprandial low-grade inflammation

Laugerette

Vors

Géloën

et al. 2011

The Journal of Nutritional Biochemistry

239

191

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Low-grade inflammation is a risk factor for the onset of atherosclerosis. Little is known about the involvement of endotoxin absorption from the gut during the digestion of lipids. In the present study, we first investigated in humans the impact of a mixed meal containing dispersed lipids on postprandial endotoxemia and inflammation. We then investigated the effect of (i) oil emulsification in vivo in rats and (ii) fatty acid amounts in vitro using Caco-2 cells on postprandial endotoxemia. In humans, postprandial endotoxemia increased early after the meal. Moreover, we evidenced that the endotoxin receptor sCD14 increased during digestion and that chylomicrons could contribute to absorbed endotoxin transport. This could explain the significant peak of inflammatory cytokine IL-6 that we observed 2 h after the mixed meal. Interestingly, in rats, the emulsion led to both higher endotoxemia and hypertriglyceridemia than oil and compared to a control saline load. In vitro, incubation of Caco-2 cells with increasing fatty acid concentrations enhanced epithelial absorption of endotoxin. To our knowledge, this is the first study evidencing in healthy humans that, following a mixed meal containing lipids, increased endotoxemia is associated with raised sCD14 and a peak of IL-6. On a repeated basis, this may thus be a triggering cascade for the onset of atherosclerosis. In this respect, optimizing both dietary fat amount and structure could be a possible strategy to limit such low-grade endotoxemia and inflammation by the control of postprandial lipemia.

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“…All the glassware used in preparation of EPAH was sterilized under 250°C for 1 h. The distilled water used for dilution of EPAH was made within 12 h. The level of endotoxin in cell culture medium and fetal calf serum was evaluated using limulus-amebocyte-lysate test (Shantou Biotechnology Inc., China) according to the method previously described [14].…”

Section: Endotoxin Controlmentioning

confidence: 99%

Oral administration of exopolysaccharide from Aphanothece halophytica (Chroococcales) significantly inhibits influenza virus (H1N1)-induced pneumonia in mice

Zheng

Chen

Cheng

et al. 2006

International Immunopharmacology

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Endotoxin release and endotoxin neutralizing capacity during colonoscopy

Cited by 18 publications

References 17 publications

A high-fat meal induces low-grade endotoxemia: evidence of a novel mechanism of postprandial inflammation

A high-fat meal induces low-grade endotoxemia: evidence of a novel mechanism of postprandial inflammation

Emulsified lipids increase endotoxemia: possible role in early postprandial low-grade inflammation

Oral administration of exopolysaccharide from Aphanothece halophytica (Chroococcales) significantly inhibits influenza virus (H1N1)-induced pneumonia in mice

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