Early enteral nutrition improves intestinal immune barrier in a rat model of severe acute pancreatitis

被引:22
作者
Peng, Lan [1 ]
Wu, Li-Guo [2 ]
Li, Bo [3 ]
Zhao, Jun [3 ]
Wen, Li-Ming [4 ]
机构
[1] Chengdu Univ, Affiliated Hosp, Dept Gastroenterol, Chengdu, Sichuan, Peoples R China
[2] Wenjiang People Hosp, Dept Gastroenterol, Chengdu, Sichuan, Peoples R China
[3] Sichuan Med Univ, Affiliated Hosp, Dept Hepatobiliary Surg, Luzhou, Sichuan, Peoples R China
[4] Dept Gastroenterol, Mianyang 404 Hosp,56 Yuejin Rd, Mianyang 621000, Sichuan, Peoples R China
关键词
Bacterial translocation; CD4+ and CD8+; Early enteral nutrition; Endotoxin; MAdCAM-1; Several acute pancreatitis; TOTAL PARENTERAL-NUTRITION; MOUSE MODEL; GUT; PERMEABILITY; INFECTION;
D O I
10.1002/jhbp.358
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
BackgroundThe aim of the present study was to investigate the role of early enteral nutrition (EEN) in the intestinal immune barrier in severe acute pancreatitis (SAP), and to explore its potential mechanisms. MethodsSixty rats were randomly assigned to three groups: sham-operated group (SO group, n=20), SAP group receiving EEN (SAP+EEN group, n=20), and SAP group receiving total parental nutrition (SAP+TPN group, n=20). SAP was induced by infusion of sodium taurocholate. Rats were killed 5days after nutritional support. The pathological damage of the intestine was determined using HE staining. The expression of MAdCAM-1, CD4+, and CD8+ in Peyer's lymph nodes of the distal ilium was examined by immunohistochemistry. Serum levels of endotoxin and bacterial translocation were determined. ResultsThe survival rate in the SAP+TPN (50%) and SAP+EEN (75%) groups was significantly lower than in the SO group (100%) (P<0.05). The survival rate in the SAP+EEN group was significantly higher than in the SAP+TPN group (P<0.05). The expression of MAdCAM-1, CD4+ and CD8+ in the intestine was decreased in SAP rats. EEN significantly increased the expression of MAdCAM-1, CD4+ and CD8+ compared with TPN, accompanied by a decrease in the serum levels of endotoxin and bacterial translocation. ConclusionsEarly enteral nutrition improves intestinal immune barrier, thus reducing bacterial and endotoxin translocation and improving the survival rate in SAP rats.
引用
收藏
页码:681 / 687
页数:7
相关论文
共 31 条
[1]   Enteral versus parenteral nutrition for acute pancreatitis [J].
Al-Omran, Mohammed ;
AlBalawi, Zaina H. ;
Tashkandi, Mariam F. ;
Al-Ansary, Lubna A. .
COCHRANE DATABASE OF SYSTEMATIC REVIEWS, 2010, (01)
[2]   Role of the gut in the course of severe acute pancreatitis [J].
Ammori, BJ .
PANCREAS, 2003, 26 (02) :122-129
[3]  
BRADLEY EL, 1993, ARCH SURG-CHICAGO, V128, P586
[4]   Meta-Analysis of Enteral Nutrition versus Total Parenteral Nutrition in Patients with Severe Acute Pancreatitis [J].
Cao, Yunfei ;
Xu, Yinglong ;
Lu, Tingna ;
Gao, Feng ;
Mo, Zengnan .
ANNALS OF NUTRITION AND METABOLISM, 2008, 53 (3-4) :268-275
[5]  
Dervenis Christos, 2003, J Hepatobiliary Pancreat Surg, V10, P415, DOI 10.1007/s00534-002-0727-5
[6]  
Diseases DDBoCMAoP, 2013, CHIN J PANCREATOL, V13, P73
[7]   Total parenteral nutrition causes circumferential intestinal atrophy, remodeling of the intestinal wall, and redistribution of eosinophils in the rat gastrointestinal tract [J].
Ekelund, Mikael ;
Kristensson, Elin ;
Ekelund, Mats ;
Ekblad, Eva .
DIGESTIVE DISEASES AND SCIENCES, 2007, 52 (08) :1833-1839
[8]   Loss of enteral nutrition in a mouse model results in intestinal epithelial barrier dysfunction [J].
Feng, Yongjia ;
Ralls, Matthew W. ;
Xiao, Weidong ;
Miyasaka, Eiichi ;
Herman, Richard S. ;
Teitelbaum, Daniel H. .
BARRIERS AND CHANNELS FORMED BY TIGHT JUNCTION PROTEINS II, 2012, 1258 :71-77
[9]   Role of β7 Integrins in Intestinal Lymphocyte Homing and Retention [J].
Gorfu, G. ;
Rivera-Nieves, J. ;
Ley, K. .
CURRENT MOLECULAR MEDICINE, 2009, 9 (07) :836-850
[10]   Enteral Nutrition within 48 Hours of Admission Improves Clinical Outcomes of Acute Pancreatitis by Reducing Complications: A Meta-Analysis [J].
Li, Jie-Yao ;
Yu, Tao ;
Chen, Guang-Cheng ;
Yuan, Yu-Hong ;
Zhong, Wa ;
Zhao, Li-Na ;
Chen, Qi-Kui .
PLOS ONE, 2013, 8 (06)