Read T E, Harris H W, Grunfeld C, Feingold K R, Calhoun M C, Kane J P, Rapp J H
Department of Surgery, University of California, San Francisco 94143.
Infect Immun. 1993 Aug;61(8):3496-502. doi: 10.1128/iai.61.8.3496-3502.1993.
Chylomicrons prevent endotoxin toxicity and increase endotoxin uptake by hepatocytes. As a consequence, less endotoxin is available to activate macrophages, thereby reducing tumor necrosis factor secretion. To determine whether the chylomicron-mediated increase in hepatocellular uptake of endotoxin results in increased endotoxin excretion into bile, we examined bile after endotoxin administration. A sublethal dose (7 micrograms/kg) of 125I-endotoxin was incubated with either rat mesenteric lymph containing nascent chylomicrons (500 mg of chylomicron triglyceride per kg of body weight) or an equal volume of normal saline (controls) for 3 h and then infused into male Sprague-Dawley rats. Bile samples were collected via a common bile duct catheter for 24 h. Infusion of endotoxin incubated with chylomicrons increased biliary excretion of endotoxin by 67% at 3 h (P < or = 0.006) and by 20% at 24 h (P < or = 0.01) compared with infusion of endotoxin incubated in saline. Endotoxin activity, as measured by the Limulus assay, was not detected in the bile of test animals. However, endotoxin activity was detected after hot phenol-water extraction of bile, demonstrating that endotoxin is inactive in the presence of bile but retains bioactivity after hepatic processing. Since the majority of an intravenous endotoxin load has been shown to be cleared by the liver, acceleration of hepatocyte clearance and biliary excretion of endotoxin may represent a component of the mechanism by which chylomicrons protect against endotoxin-induced lethality.
乳糜微粒可预防内毒素毒性,并增加肝细胞对内毒素的摄取。因此,可用于激活巨噬细胞的内毒素减少,从而降低肿瘤坏死因子的分泌。为了确定乳糜微粒介导的肝细胞对内毒素摄取的增加是否会导致内毒素向胆汁中的排泄增加,我们在内毒素给药后检查了胆汁。将亚致死剂量(7微克/千克)的125I-内毒素与含有新生乳糜微粒的大鼠肠系膜淋巴(每千克体重500毫克乳糜微粒甘油三酯)或等体积的生理盐水(对照组)孵育3小时,然后注入雄性Sprague-Dawley大鼠体内。通过胆总管导管收集胆汁样本24小时。与注入在盐水中孵育的内毒素相比,注入与乳糜微粒孵育的内毒素在3小时时使胆汁内毒素排泄增加67%(P≤0.006),在24小时时增加20%(P≤0.01)。在用鲎试剂法测定时,在受试动物的胆汁中未检测到内毒素活性。然而,在对胆汁进行热酚-水提取后检测到了内毒素活性,这表明内毒素在胆汁存在时无活性,但在肝脏处理后保留生物活性。由于已表明静脉内注入的大部分内毒素负荷可被肝脏清除,加速肝细胞对内毒素的清除和胆汁排泄可能是乳糜微粒预防内毒素诱导的致死性机制的一个组成部分。