Host-bacteria interactions in the intestine: homeostasis to chronic inflammation

被引:27
作者
Barbosa, Theolis [1 ]
Rescigno, Maria [1 ]
机构
[1] European Inst Oncol, Dept Expt Oncol, Milan, Italy
关键词
GENOME-WIDE ASSOCIATION; TOLL-LIKE RECEPTORS; REGULATORY T-CELLS; MUCOSAL IMMUNE-RESPONSES; NEONATAL FC-RECEPTOR; BOWEL-DISEASE; CROHNS-DISEASE; EPITHELIAL-CELLS; ULCERATIVE-COLITIS; TGF-BETA;
D O I
10.1002/wsbm.48
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
In the past decade it has become clear that the gut constitutes an important frontier of the body, which not only regulates the selective entry of nutrients while keeping vigilant against pathogens but also is largely responsible for shaping the immune response to educate the organism to recognize self from non-self. The very notion of self has undergone a dramatic change, with the acknowledgment that our 'selves' include a plethora of microbial species that actively participate in our body's homeostasis. The immune system continuously adapts to the microbiota in a cyclic, dynamic cross talk where intestinal epithelial cells play an important role in instructing noninflammatory responses for a steady-state control of bacterial growth, or triggering inflammatory mechanisms that can clear the gut from harmful invaders. The system is complex and robust in the sense that many players with partially overlapping roles act to keep the integrity of the intestinal mucosal barrier. Failure of these mechanisms involves genetic and environmental triggers and leads to inflammatory bowel disease. In this review, we seek to collect the state-of-the-art knowledge about how host and microbiota interact to promote gut homeostasis and provide evidences of malfunctioning of the described mechanisms in human inflammatory bowel disease. (C) 2009 John Wiley & Sons, Inc. WIREs Syst Biol Med 2010 2 80-97
引用
收藏
页码:80 / 97
页数:18
相关论文
共 152 条
[1]  
Amit-Romach E, 2006, INT J MOL MED, V18, P721
[2]   IL-17 selectively down-regulates TNF-α-induced RANTES gene expression in human colonic subepithelial myofibroblasts [J].
Andoh, A ;
Fujino, S ;
Bamba, S ;
Araki, Y ;
Okuno, T ;
Bamba, T ;
Fujiyama, Y .
JOURNAL OF IMMUNOLOGY, 2002, 169 (04) :1683-1687
[3]   MyD88-deficient mice develop severe intestinal inflammation in dextran sodium sulfate colitis [J].
Araki, A ;
Kanai, T ;
Ishikura, T ;
Makita, S ;
Uraushihara, K ;
Iiyama, R ;
Totsuka, T ;
Takeda, K ;
Akira, S ;
Watanabe, M .
JOURNAL OF GASTROENTEROLOGY, 2005, 40 (01) :16-23
[4]   Enterococcus faecalis from newborn babies regulate endogenous PPARγ activity and IL-10 levels in colonic epithelial cells [J].
Are, Alexandra ;
Aronsson, Linda ;
Wang, Shugui ;
Greicius, Gediminas ;
Lee, Yuan Kun ;
Gustafsson, Jan-Ake ;
Pettersson, Sven ;
Arulampalam, Velmurugesan .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2008, 105 (06) :1943-1948
[5]   Epithelial-cell recognition of commensal bacteria and maintenance of immune homeostasis in the gut [J].
Artis, David .
NATURE REVIEWS IMMUNOLOGY, 2008, 8 (06) :411-420
[6]   ATP drives lamina propria TH17 cell differentiation [J].
Atarashi, Koji ;
Nishimura, Junichi ;
Shima, Tatsuichiro ;
Umesaki, Yoshinori ;
Yamamoto, Masahiro ;
Onoue, Masaharu ;
Yagita, Hideo ;
Ishii, Naoto ;
Evans, Richard ;
Honda, Kenya ;
Takeda, Kiyoshi .
NATURE, 2008, 455 (7214) :808-U10
[7]   The adherent gastrointestinal mucus gel layer: thickness and physical state in vivo [J].
Atuma, C ;
Strugala, V ;
Allen, A ;
Holm, L .
AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY, 2001, 280 (05) :G922-G929
[8]   Chemokine expression in IBD. Mucosal chemokine expression is unselectively increased in both ulcerative colitis and Crohn's disease [J].
Banks, C ;
Bateman, A ;
Payne, R ;
Johnson, P ;
Sheron, N .
JOURNAL OF PATHOLOGY, 2003, 199 (01) :28-35
[9]   A genome scan in 260 inflammatory bowel disease-affected relative pairs [J].
Barmada, MM ;
Brant, SR ;
Nicolae, DL ;
Achkar, JP ;
Panhuysen, CI ;
Bayless, TM ;
Cho, JH ;
Duerr, RH .
INFLAMMATORY BOWEL DISEASES, 2004, 10 (05) :513-520
[10]   Genome-wide association defines more than 30 distinct susceptibility loci for Crohn's disease [J].
Barrett, Jeffrey C. ;
Hansoul, Sarah ;
Nicolae, Dan L. ;
Cho, Judy H. ;
Duerr, Richard H. ;
Rioux, John D. ;
Brant, Steven R. ;
Silverberg, Mark S. ;
Taylor, Kent D. ;
Barmada, M. Michael ;
Bitton, Alain ;
Dassopoulos, Themistocles ;
Datta, Lisa Wu ;
Green, Todd ;
Griffiths, Anne M. ;
Kistner, Emily O. ;
Murtha, Michael T. ;
Regueiro, Miguel D. ;
Rotter, Jerome I. ;
Schumm, L. Philip ;
Steinhart, A. Hillary ;
Targan, Stephan R. ;
Xavier, Ramnik J. ;
Libioulle, Cecile ;
Sandor, Cynthia ;
Lathrop, Mark ;
Belaiche, Jacques ;
Dewit, Olivier ;
Gut, Ivo ;
Heath, Simon ;
Laukens, Debby ;
Mni, Myriam ;
Rutgeerts, Paul ;
Van Gossum, Andre ;
Zelenika, Diana ;
Franchimont, Denis ;
Hugot, Jean-Pierre ;
de Vos, Martine ;
Vermeire, Severine ;
Louis, Edouard ;
Cardon, Lon R. ;
Anderson, Carl A. ;
Drummond, Hazel ;
Nimmo, Elaine ;
Ahmad, Tariq ;
Prescott, Natalie J. ;
Onnie, Clive M. ;
Fisher, Sheila A. ;
Marchini, Jonathan ;
Ghori, Jilur .
NATURE GENETICS, 2008, 40 (08) :955-962