Chylomicrons promote intestinal absorption of lipopolysaccharides

Chylomicrons promote intestinal absorption of lipopolysaccharides
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DOI:
10.1194/jlr.m800156-jlr200
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发表时间:
2009-01-01
影响因子:
6.5
通讯作者:
Eckhardt, Erik
Eckhardt, Erik
中科院分区:
生物学2区
文献类型:
--
作者:
Ghoshal, Sarbani;Witta, Jassir;Eckhardt, Erik

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最近的数据表明,膳食脂肪促进肠吸收的脂多糖(LPS)从肠道微生物,这可能有助于各种炎症性疾病。然而,脂肪诱导的LPS吸收的机制尚不清楚。肠上皮细胞可以从顶端表面内化LPS并将LPS转运到高尔基体。高尔基复合体还含有新形成的乳糜微粒,这些脂蛋白通过肠系膜淋巴和血液运输膳食长链脂肪。由于LPS对乳糜微粒具有亲和力,我们假设乳糜微粒的形成促进LPS的吸收。与我们的假设一致,我们发现CaCo-2细胞与油酸(OA)(一种诱导乳糜微粒形成的长链脂肪酸)孵育后释放的细胞相关LPS比与丁酸(BA)(一种不诱导乳糜微粒形成的短链脂肪酸)孵育后释放的细胞相关LPS更多。乳糜微粒形成。此外,OA的作用被乳糜微粒形成抑制剂Pluronic L-81阻断。我们还观察到,胃内三油酸甘油酯(TO)灌胃后,血浆LPS增加,而灌胃三丁酸甘油酯(TB),或TO加普朗尼克L-81,没有。大多数肠道吸收的LPS存在于血液中的乳糜微粒残留物(CM-R)上。乳糜微粒的形成也促进了LPS通过肠系膜淋巴结(MLN)的转运和MLN中TNF α mRNA的产生。总之,我们的数据表明,肠上皮细胞可能会释放脂多糖乳糜微粒从细胞相关池。乳糜微粒相关的LPS可能有助于乳糜微粒靶组织的餐后炎症反应或慢性饮食诱导的炎症。戈沙尔,S.,J. Witta,J. Zhong,W. de Villiers和E.埃克哈特乳糜微粒促进脂多糖的肠吸收。J. Lipid Res. 2009. 50:90-97.
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 long-chain 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 TNF alpha 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.