The intestinal microbiota dysbiosis and Clostridium difficile infection: is there a relationship with inflammatory bowel disease?

被引:172
作者
Bien, Justyna [2 ]
Palagani, Vindhya [1 ]
Bozko, Przemyslaw [1 ]
机构
[1] Univ Tubingen, Dept Internal Med 1, Fac Med, D-72076 Tubingen, Germany
[2] Polish Acad Sci, Witold Stefanski Inst Parasitol, Warsaw, Poland
关键词
Clostridium difficile; inflammatory bowel disease; microbial dysbiosis; 16S RIBOSOMAL-RNA; NF-KAPPA-B; ACID-SUPPRESSIVE AGENTS; TOXIN-B; SIGNALING PATHWAYS; FECAL MICROBIOTA; EGF RECEPTOR; ACTIVATION; DIVERSITY; DIARRHEA;
D O I
10.1177/1756283X12454590
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Gut microbiota is a compilation of microorganisms dwelling in the entire mammalian gastrointestinal tract. They display a symbiotic relationship with the host contributing to its intestinal health and disease. Even a slight fluctuation in this equipoise may be deleterious to the host, leading to many pathological conditions like Clostridium difficile infection or inflammatory bowel disease (IBD). In this review, we focus on the role of microbial dysbiosis in initiation of C. difficile infection and IBD, and we also touch upon the role of specific pathogens, particularly C. difficile, as causative agents of IBD. We also discuss the molecular mechanisms activated by C. difficile that contribute to the development and exacerbation of gastrointestinal disorders.
引用
收藏
页码:53 / 68
页数:16
相关论文
共 131 条
[51]  
Jefferson KK, 1999, J IMMUNOL, V163, P5183
[52]   Long-term ecological impacts of antibiotic administration on the human intestinal microbiota [J].
Jernberg, Cecilia ;
Lofmark, Sonja ;
Edlund, Charlotta ;
Jansson, Janet K. .
ISME JOURNAL, 2007, 1 (01) :56-66
[53]   GLUCOSYLATION OF RHO-PROTEINS BY CLOSTRIDIUM-DIFFICILE TOXIN-B [J].
JUST, I ;
SELZER, J ;
WILM, M ;
VONEICHELSTREIBER, C ;
MANN, M ;
AKTORIES, K .
NATURE, 1995, 375 (6531) :500-503
[54]   CLOSTRIDIUM DIFFICILE TOXIN IN ACUTE DIARRHEA COMPLICATING INFLAMMATORY BOWEL-DISEASE [J].
KEIGHLEY, MRB ;
YOUNGS, D ;
JOHNSON, M ;
ALLAN, RN ;
BURDON, DW .
GUT, 1982, 23 (05) :410-414
[55]  
Kelly CP, 1998, ANNU REV MED, V49, P375
[56]   Clostridium difficile toxin A regulates inducible cyclooxygenase-2 and prostaglandin E2 synthesis in colonocytes via reactive oxygen species and activation of p38 MAPK [J].
Kim, H ;
Rhee, SH ;
Kokkotou, E ;
Na, X ;
Savidge, T ;
Moyer, MP ;
Pothoulakis, C ;
LaMont, JT .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2005, 280 (22) :21237-21245
[57]   NF-κB activation pathway is essential for the chemokine expression in intestinal epithelial cells stimulated with Clostridium difficile toxin A [J].
Kim, J. M. ;
Lee, J. Y. ;
Yoon, Y. M. ;
Oh, Y. -K. ;
Youn, J. ;
Kim, Y. -J. .
SCANDINAVIAN JOURNAL OF IMMUNOLOGY, 2006, 63 (06) :453-460
[58]  
Kobayashi T, 1983, Jpn J Antibiot, V36, P464
[59]   Activation of MMP-2 by Clostridium difficile toxin B in bovine smooth muscle cells [J].
Koike, T ;
Kuzuya, M ;
Asai, T ;
Kanda, S ;
Cheng, XW ;
Watanabe, K ;
Banno, Y ;
Nozawa, Y ;
Iguchi, A .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2000, 277 (01) :43-46
[60]   CELL-SURFACE BINDING-SITE FOR CLOSTRIDIUM-DIFFICILE ENTEROTOXIN - EVIDENCE FOR A GLYCOCONJUGATE CONTAINING THE SEQUENCE GAL-ALPHA-1-3GAL-BETA-1-4GLCN AC [J].
KRIVAN, HC ;
CLARK, GF ;
SMITH, DF ;
WILKINS, TD .
INFECTION AND IMMUNITY, 1986, 53 (03) :573-581