Increased ICAM-1 and β2 integrin expression in parenterally fed mice after a gut ischemic insult
Increased ICAM-1 and β2 integrin expression in parenterally fed mice after a gut ischemic insult
复制标题
DOI：
10.1097/00024382-200208000-00005
复制
发表时间：
2002-08-01
期刊：
影响因子：
3.1
通讯作者：
Johnson, CD
中科院分区：
文献类型：
--
作者：
Fukatsu, K;Kudsk, KA;Johnson, CD
肠内喂养的缺乏增加了器官（如小肠和肺）中内皮细胞上的P-和E-选择素以及ICAM-1的表达，并增加了肠中的中性粒细胞。这些变化与肠缺血后死亡率增加有关。我们假设营养方案影响肠缺血后内皮细胞ICAM-1水平和白细胞β 2整合素。小鼠接受饲料、静脉内（IV）TPN或胃内（IG）TPN。实验1中，28只小鼠在饮食5天后经历15 min的上级肠系膜动脉（SMA）闭塞（I/R），以在3 h后定量器官中ICAM-1的表达。实验2中，38只小鼠经相同的营养素预处理后，在有或没有肠道I/R的情况下获得外周血，以测量骨髓细胞上的CD 11 a和CD 11b表达。对肺组织进行CD 18免疫荧光染色。IV-TPN后肝、肾、小肠ICAM-1的表达明显高于对照组。IG-TPN降低了食物组和IV-TPN组之间的肝脏和肾脏ICAM-1水平，但不降低肠道表达。I/R前各组骨髓细胞群上的CD 11b表达相似，但与所有未受伤动物或受伤的食物或IG-TPN小鼠相比，I/R后IV-TPN后循环细胞上的CD 11b水平升高。仅IV-TPN小鼠在I/R后出现肺CD 18阳性白细胞。I/R后，缺乏肠内喂养增加了器官ICAM-1的表达、髓系细胞上的CD 11b水平和CD 18阳性白细胞的肺。通过这些变化，缺乏肠道喂养可能会增加肠道缺血后的器官损伤。
Lack of enteral feeding increases P- and E-selectin and ICAM-1 expression on endothelial cells in organs, such as the small intestine and lung, and increases neutrophils in the intestine. These changes are associated with increased mortality after gut ischemia. We hypothesize that nutritional regimen affects endothelial ICAM-1 levels and leukocyte beta2 integrins after gut ischemia. Mice received chow, intravenous (IV) TPN, or intragastric (IG) TPN. In experiment 1, after 5 days of diet, 28 mice underwent 15 min of superior mesenteric artery (SMA) occlusion (I/R) for quantification of ICAM-1 expression in organs 3 h later. In experiment 2, after the same nutrient pretreatments of 38 mice, peripheral blood was obtained with or without gut I/R to measure CD11a and CD11b expression on myeloid cells. CD18 immunofluorescence staining was studied in the lung. Expression of ICAM-1 in the liver, kidney, and small intestine was significantly higher after IV-TPN than chow. IG-TPN reduced liver and kidney ICAM-1 levels midway between the chow and IV-TPN groups, but not intestinal expression. Expression of CD11b on the myeloid cell population in each group was similar before I/R, but CD11b levels increased after IV-TPN on circulating cells after I/R compared with all uninjured animals or injured chow or IG-TPN mice. Only IV-TPN mice had lung CD18-positive leukocytes after I/R. After I/R, lack of enteral feeding increases organ expression of ICAM-1, CD11b levels on myeloid cells, and lung of CD18 positive leukocytes. Through these changes, lack of enteral feeding may increase organ damage after gut ischemia.