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
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DOI：
10.1093/ajcn/86.5.1286
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发表时间：
2007-11-01
影响因子：
7.1
通讯作者：
Webb, David J.
中科院分区：
文献类型：
--
作者：
Erridge, Clett;Attina, Teresa;Webb, David J.
背景：细菌内毒素是一种强有力的炎症抗原，在人体肠道中大量存在。内毒素循环在低浓度的血液中的所有健康个体，虽然浓度升高与动脉粥样硬化的风险增加。目的：我们试图确定是否高脂肪餐或吸烟增加血浆内毒素浓度，以及是否这样的浓度是生理相关性。设计图：用鲎试剂法测定了12名健康男性空腹、3支香烟、高脂餐及高脂餐加3支香烟后4 h血浆内毒素及内毒素中和能力（四分位数范围：3.4-13.5 pg/mL），但在高脂餐后或在高脂餐伴香烟后显著增加（P < 0.05），约50%，但在不进餐或仅吸烟后不增加。这些结果通过以下观察得到验证：高脂肪餐伴或不伴香烟，但不伴或不吸烟，也显著（P < 0.05）降低血浆内毒素中和能力，这是内毒素暴露的间接测量。人单核细胞，而不是主动脉内皮细胞，对短暂（30秒）或低剂量（10 pg/mL）暴露于内毒素有反应。然而，血浆从全血处理低至10 pg内毒素/mL的E-选择素的内皮细胞表达增加，至少部分通过肿瘤坏死因子-α-诱导的细胞activation.Conclusions：低级别的内毒素血症可能有助于餐后炎症状态，并可能代表一种新的潜在的贡献者内皮激活和动脉粥样硬化的发展。
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 approximate to 50% 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 low-dose (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-alpha-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.