The use of animal models to study bacterial translocation during acute pancreatitis

被引:66
作者
van Minnen, L. P.
Blom, M.
Timmerman, H. M.
Visser, M. R.
Gooszen, H. G.
Akkermans, L. M. A.
机构
[1] Univ Med Ctr Utrecht, Dept Surg, Gastrointestinal Res Unit, NL-3508 GA Utrecht, Netherlands
[2] Univ Med Ctr Utrecht, Dept Med Microbiol, Utrecht, Netherlands
关键词
pancreatitis; bacterial translocation; animal; model;
D O I
10.1007/s11605-007-0088-0
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Infection of pancreatic necrosis with intestinal flora is accepted to be a main predictor of outcome during severe acute pancreatitis. Bacterial translocation is the process whereby luminal bacteria migrate to extraintestinal sites. Animal models were proven indispensable in detecting three major aspects of bacterial translocation: small bowel bacterial overgrowth, mucosal barrier failure, and disturbed immune responses. Despite the progress made in the knowledge of bacterial translocation, the exact mechanism, origin and route of bacteria, and the optimal prophylactic and treatment strategies remain unclear. Methodological restrictions of animal models are likely to be the cause of this uncertainty. A literature review of animal models used to study bacterial translocation during acute pancreatitis demonstrates that many experimental techniques per se interfere with intestinal flora, mucosal barrier function, or immune response. Interference with these major aspects of bacterial translocation complicates interpretation of study results. This paper addresses these and other issues of animal models most frequently used to study bacterial translocation during acute pancreatitis.
引用
收藏
页码:682 / 689
页数:8
相关论文
共 79 条
[31]   BACTERIAL TRANSLOCATION - A POTENTIAL SOURCE FOR INFECTION IN ACUTE-PANCREATITIS [J].
GIANOTTI, L ;
MUNDA, R ;
ALEXANDER, JW ;
TCHERVENKOV, JI ;
BABCOCK, GF .
PANCREAS, 1993, 8 (05) :551-558
[32]   Late mortality in patients with severe acute pancreatitis [J].
Gloor, B ;
Müller, CA ;
Worni, M ;
Martignoni, ME ;
Uhl, W ;
Büchler, MW .
BRITISH JOURNAL OF SURGERY, 2001, 88 (07) :975-979
[33]  
GUSTAFSSON BE, 1960, P SOC EXP BIOL MED, V104, P319, DOI 10.3181/00379727-104-25821
[34]   Effects of fasting and refeeding on jejunal morphology and cellular activity in rats in relation to depletion of body stores [J].
Habold, C ;
Chevalier, C ;
Dunel-Erb, S ;
Foltzer-Jourdainne, C ;
Le Maho, Y ;
Lignot, JH .
SCANDINAVIAN JOURNAL OF GASTROENTEROLOGY, 2004, 39 (06) :531-539
[35]   Further evidence for endothelin as an important mediator of pancreatic and intestinal ischemia in severe acute pancreatitis [J].
Inoue, K ;
Hirota, M ;
Kimura, Y ;
Kuwata, K ;
Ohmuraya, M ;
Ogawa, M .
PANCREAS, 2003, 26 (03) :218-223
[36]  
JILGE B, 1975, Z VERSUCHSTIERKD, V17, P308
[37]   PLASMID LABELING CONFIRMS BACTERIAL TRANSLOCATION IN PANCREATITIS [J].
KAZANTSEV, GB ;
HECHT, DW ;
RAO, R ;
FEDORAK, IJ ;
GATTUSO, P ;
THOMPSON, K ;
DJURICIN, G ;
PRINZ, RA .
AMERICAN JOURNAL OF SURGERY, 1994, 167 (01) :201-207
[38]   ACUTE INTERSTITIAL PANCREATITIS IN RAT INDUCED BY EXCESSIVE DOSES OF A PANCREATIC SECRETAGOGUE [J].
LAMPEL, M ;
KERN, HF .
VIRCHOWS ARCHIV A-PATHOLOGICAL ANATOMY AND HISTOPATHOLOGY, 1977, 373 (02) :97-117
[39]   WHEN SHOULD TREATMENT OF ACUTE EXPERIMENTAL PANCREATITIS BE STARTED - THE EARLY PHASE OF BILE-INDUCED ACUTE-PANCREATITIS [J].
LANKISCH, PG ;
POHL, U ;
OTTO, J ;
RAHLF, G .
RESEARCH IN EXPERIMENTAL MEDICINE, 1988, 188 (02) :123-129
[40]   LUMINAL ENDOCYTOSIS AND INTRACELLULAR TARGETING BY ACINAR-CELLS DURING EARLY BILIARY PANCREATITIS IN THE OPOSSUM [J].
LERCH, MM ;
SALUJA, AK ;
RUNZI, M ;
DAWRA, R ;
STEER, ML .
JOURNAL OF CLINICAL INVESTIGATION, 1995, 95 (05) :2222-2231