Lipopolysaccharides (LPS) transport during fat absorption in rodent small intestine.
Lipopolysaccharides (LPS) transport during fat absorption in rodent small intestine.
复制标题
啮齿动物小肠脂肪吸收过程中脂多糖（LPS）的运输。
DOI：
--
复制
发表时间：
2020
期刊：
影响因子：
--
通讯作者：
J. Kaunitz
中科院分区：
文献类型：
--
作者：
Y. Akiba;K. Maruta;Takeshi Takajo;K. Narimatsu;Hyder Said;I. Kato;A. Kuwahara;J. Kaunitz
脂多糖（LPS）是一种强效的促炎分子，通过不确定的机制从肠腔进入体循环。我们研究了这些机制以及外源性胰高血糖素样肽-2 （GLP-2）对LPS在啮齿动物小肠内转运的影响。测定了大鼠空肠粘膜脂多糖的经黏膜转运。在麻醉大鼠十二指肠内灌注油酸和牛磺酸胆酸（OA/TCA）后，同时监测FITC-LPS进入门静脉（PV）和肠系膜淋巴的情况。在体外，光施LPS仅在存在OA/TCA的浆膜溶液中迅速出现，被脂质raft抑制剂甲基β-环糊精（m -β- cd）和CD36抑制剂磺基琥珀酰油酸酯（SSO）或浆膜GLP-2抑制。在体内，OA/TCA灌注FITC-LPS可迅速增加FITC-LPS进入PV的外观，随后进入淋巴的FITC-LPS逐渐增加。添加m - β cd或SSO可抑制PV的快速转运，而乳糜微粒合成抑制则可抑制PV进入淋巴的转运。静脉注射稳定的GLP-2类似物特杜葡肽急性抑制PV中FITC-LPS向PV的转运，但通过L-NAME和pg97 -269敏感机制加速FITC-LPS向淋巴的转运。小鼠空肠的体内共聚焦显微镜证实了细胞内FITC-LPS摄取，没有细胞旁定位的证据。这是第一次在体内直接证明，在脂肪吸收过程中，内源性LPS可以通过脂质筏和cd36介导的机制生理地穿过小肠屏障，然后主要转运到PV中，并且teduglutide在体内抑制LPS摄取到PV中。
Lipopolysaccharides (LPS) are potent pro-inflammatory molecules that enter the systemic circulation from the intestinal lumen by uncertain mechanisms. We investigated these mechanisms and the effect of exogenous glucagon-like peptide-2 (GLP-2) on LPS transport in rodent small intestine. Transmucosal LPS transport was measured in Ussing-chambered rat jejunal mucosa. In anesthetized rats, the appearance of FITC-LPS into the portal vein (PV) and the mesenteric lymph was simultaneously monitored after intraduodenal perfusion of FITC-LPS with oleic acid and taurocholate (OA/TCA). In vitro, luminally-applied LPS rapidly appeared in the serosal solution only with luminal OA/TCA present, inhibited by the lipid raft inhibitor methyl-β-cyclodextrin (MβCD) and the CD36 inhibitor sulfosuccinimidyl oleate (SSO), or by serosal GLP-2. In vivo, perfusion of FITC-LPS with OA/TCA rapidly increased FITC-LPS appearance into the PV, followed by a gradual increase of FITC-LPS into the lymph. Rapid PV transport was inhibited by the addition of MβCD or by SSO, whereas transport into the lymph was inhibited by chylomicron synthesis inhibition. IV injection of the stable GLP-2 analog teduglutide acutely inhibited PV FITC-LPS transport into the PV, yet accelerated FITC-LPS transport into the lymph via L-NAME- and PG97-269-sensitive mechanisms. In vivo confocal microscopy in mouse jejunum confirmed intracellular FITC-LPS uptake with no evidence of paracellular localization. This is the first direct demonstration in vivo that luminal LPS may cross the small intestinal barrier physiologically during fat absorption via lipid raft- and CD36-mediated mechanisms, followed by predominant transport into the PV, and that teduglutide inhibits LPS uptake into the PV in vivo.
登录
查看更多内容
影响因子：
--
作者：
KVIETYS, PR;SPECIAN, RD;TSO, P
通讯作者：
TSO, P
影响因子：
2.2
作者：
EICHBAUM, EB;HARRIS, HW;RAPP, JH
通讯作者：
RAPP, JH
DOI：
10.1152/ajpgi.00163.2009
发表时间：
2011-03-01
影响因子：
4.5
作者：
Csak, Timea;Velayudham, Arumugam;Szabo, Gyongyi
通讯作者：
Szabo, Gyongyi
影响因子：
29.4
作者：
D. Granger;M. Perry;P. Kvietys;A. Taylor
通讯作者：
D. Granger;M. Perry;P. Kvietys;A. Taylor
DOI：
--
发表时间：
1997-11
期刊：
Clinical cancer research : an official journal of the American Association for Cancer Research
影响因子：
--
作者：
Monique Bos;John Mendelsohn;Young Mee Kim;Joan Albanell;David W. Fry;David W. Fry;José Baselga
通讯作者：
Monique Bos;John Mendelsohn;Young Mee Kim;Joan Albanell;David W. Fry;David W. Fry;José Baselga