Intestinal barrier in inflammatory bowel disease

被引:468
作者
Antoni, Lena [1 ]
Nuding, Sabine [1 ]
Wehkamp, Jan [1 ,2 ]
Stange, Eduard F. [2 ]
机构
[1] Univ Tubingen, Dr Margarete Fischer Bosch Inst Clin Pharmacol, D-70376 Stuttgart, Germany
[2] Robert Bosch Krankenhaus, Dept Internal Med 1, D-70376 Stuttgart, Germany
关键词
Intestinal barrier; Antimicrobial peptide; Mucus layer; Inflammatory bowel disease; Crohn's disease; Ulcerative colitis; Goblet cell; Paneth cell; INVASIVE ESCHERICHIA-COLI; EPITHELIAL TIGHT JUNCTIONS; ILEAL CROHNS-DISEASE; CELL ALPHA-DEFENSINS; 2 MUCUS LAYERS; ULCERATIVE-COLITIS; ANTIMICROBIAL PEPTIDES; INNATE IMMUNITY; HOST-DEFENSE; PANETH CELLS;
D O I
10.3748/wjg.v20.i5.1165
中图分类号
R57 [消化系及腹部疾病];
学科分类号
100201 [内科学];
摘要
A complex mucosal barrier protects as the first line of defense the surface of the healthy intestinal tract from adhesion and invasion by luminal microorganisms. In this review, we provide an overview about the major components of this protective system as for example an intact epithelium, the synthesis of various antimicrobial peptides (AMPs) and the formation of the mucus layer. We highlight the crucial importance of their correct functioning for the maintenance of a proper intestinal function and the prevention of dysbiosis and disease. Barrier disturbances including a defective production of AMPs, alterations in thickness or composition of the intestinal mucus layer, alterations of pattern-recognition receptors, defects in the process of autophagy as well as unresolved endoplasmic reticulum stress result in an inadequate host protection and are thought to play a crucial role in the pathogenesis of the inflammatory bowel diseases Crohn's disease and ulcerative colitis. (C) 2014 Baishideng Publishing Group Co., Limited. All rights reserved.
引用
收藏
页码:1165 / 1179
页数:15
相关论文
共 170 条
[1]
The MUC2 gene product: a human intestinal mucin [J].
Allen, A ;
Hutton, DA ;
Pearson, JP .
INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY, 1998, 30 (07) :797-801
[2]
Perspectives on Mucus Properties and Formation-Lessons from the Biochemical World [J].
Ambort, Daniel ;
Johansson, Malin E. V. ;
Gustafsson, Jenny K. ;
Ermund, Anna ;
Hansson, Gunnar C. .
COLD SPRING HARBOR PERSPECTIVES IN MEDICINE, 2012, 2 (11)
[3]
Antoni Lena, 2013, J Crohns Colitis, V7, pe652, DOI 10.1016/j.crohns.2013.05.006
[4]
Arnott IDR, 2000, SCAND J GASTROENTERO, V35, P1163
[5]
51CrEDTA colonic permeability and therapy response in patients with ulcerative colitis [J].
Arslan, G ;
Atasever, T ;
Cindoruk, M ;
Yildirim, IS .
NUCLEAR MEDICINE COMMUNICATIONS, 2001, 22 (09) :997-1001
[6]
Multifunctional host defense peptides: Antimicrobial peptides, the small yet big players in innate and adaptive immunity [J].
Auvynet, Constance ;
Rosenstein, Yvonne .
FEBS JOURNAL, 2009, 276 (22) :6497-6508
[7]
CEACAM6 acts as a receptor for adherent-invasive E. coli, supporting ileal mucosa colonization in Crohn disease [J].
Barnich, Nicolas ;
Carvalho, Frederic A. ;
Glasser, Anne-Lise ;
Darcha, Claude ;
Jantscheff, Peter ;
Allez, Matthieu ;
Peeters, Harald ;
Bommelaer, Gilles ;
Desreumaux, Pierre ;
Colombel, Jean-Frederic ;
Darfeuille-Michaud, Arlette .
JOURNAL OF CLINICAL INVESTIGATION, 2007, 117 (06) :1566-1574
[8]
Colitis induced in mice with dextran sulfate sodium (DSS) is mediated by the NLRP3 inflammasome [J].
Bauer, Christian ;
Duewell, Peter ;
Mayer, Christine ;
Lehr, Hans Anton ;
Fitzgerald, Katherine A. ;
Dauer, Marc ;
Tschopp, Jurg ;
Endres, Stefan ;
Latz, Eicke ;
Schnurr, Max .
GUT, 2010, 59 (09) :1192-1199
[9]
The c.1-260C>T promoter variant of CD14 but not the c.896A>G (p.D299G) variant of toll-like receptor 4 (TLR4) genes is associated with inflammatory bowel disease [J].
Baumgart, Daniel C. ;
Buening, Carsten ;
Geerdts, Lars ;
Schmidt, Hartmut H. ;
Genschel, Janine ;
Fiedler, Thomas ;
Gentz, Enno ;
Molnar, Tomas ;
Nagy, Ferenc ;
Lonovics, Janos ;
Lochs, Herbert ;
Wiedenmann, Bertram ;
Nickel, Renate ;
Witt, Heiko ;
Dignass, Axel .
DIGESTION, 2007, 76 (3-4) :196-202
[10]
Increased sensitivity to dextran sodium sulfate colitis in IRE1β-deficient mice [J].
Bertolotti, A ;
Wang, XZ ;
Novoa, I ;
Jungreis, R ;
Schlessinger, K ;
Cho, JH ;
West, AB ;
Ron, D .
JOURNAL OF CLINICAL INVESTIGATION, 2001, 107 (05) :585-593