Inflammatory bowel disease: Pathogenesis

被引:1453
作者
Zhang, Yi-Zhen [1 ]
Li, Yong-Yu [1 ]
机构
[1] Tongji Univ, Sch Med, Dept Pathophysiol, Shanghai 200092, Peoples R China
基金
中国国家自然科学基金;
关键词
Inflammatory bowel disease; Ulcerative colitis; Crohn's disease; pathogenesis; Genetics; Microbial factors; Immune responses; GENOME-WIDE ASSOCIATION; INVASIVE ESCHERICHIA-COLI; AMBIENT AIR-POLLUTION; NOD2; CARD15; MUTATIONS; CROHNS-DISEASE; ULCERATIVE-COLITIS; THERAPEUTIC IMPLICATIONS; PSYCHOLOGICAL STRESS; SUSCEPTIBILITY LOCI; FUTURE-DIRECTIONS;
D O I
10.3748/wjg.v20.i1.91
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
Inflammatory bowel disease (IBD), including Crohn's disease and ulcerative colitis, is characterized by chronic relapsing intestinal inflammation. It has been a worldwide health-care problem with a continually increasing incidence. It is thought that IBD results from an aberrant and continuing immune response to the microbes in the gut, catalyzed by the genetic susceptibility of the individual. Although the etiology of IBD remains largely unknown, it involves a complex interaction between the genetic, environmental or microbial factors and the immune responses. Of the four components of IBD pathogenesis, most rapid progress has been made in the genetic study of gut inflammation. The latest internationally collaborative studies have ascertained 163 susceptibility gene loci for IBD. The genes implicated in childhood-onset and adult-onset IBD overlap, suggesting similar genetic predispositions. However, the fact that genetic factors account for only a portion of overall disease variance indicates that microbial and environmental factors may interact with genetic elements in the pathogenesis of IBD. Meanwhile, the adaptive immune response has been classically considered to play a major role in the pathogenesis of IBD, as new studies in immunology and genetics have clarified that the innate immune response maintains the same importance in inducing gut inflammation. Recent progress in understanding IBD pathogenesis sheds lights on relevant disease mechanisms, including the innate and adaptive immunity, and the interactions between genetic factors and microbial and environmental cues. In this review, we provide an update on the major advances that have occurred in above areas. (C) 2014 Baishideng Publishing Group Co., Limited. All rights reserved.
引用
收藏
页码:91 / 99
页数:9
相关论文
共 93 条
[1]
Functional consequences of NOD2 (CARD15) mutations [J].
Abraham, Clara ;
Cho, Judy H. .
INFLAMMATORY BOWEL DISEASES, 2006, 12 (07) :641-650
[2]
MECHANISMS OF DISEASE Inflammatory Bowel Disease [J].
Abraham, Clara ;
Cho, Judy H. .
NEW ENGLAND JOURNAL OF MEDICINE, 2009, 361 (21) :2066-2078
[3]
TLR signaling in the gut in health and disease [J].
Abreu, MT ;
Fukata, M ;
Arditi, M .
JOURNAL OF IMMUNOLOGY, 2005, 174 (08) :4453-4460
[4]
Aspirin, Nonsteroidal Anti-inflammatory Drug Use, and Risk for Crohn Disease and Ulcerative Colitis A Cohort Study [J].
Ananthakrishnan, Ashwin N. ;
Higuchi, Leslie M. ;
Huang, Edward S. ;
Khalili, Hamed ;
Richter, James M. ;
Fuchs, Charles S. ;
Chan, Andrew T. .
ANNALS OF INTERNAL MEDICINE, 2012, 156 (05) :350-U170
[5]
Ambient Air Pollution Correlates with Hospitalizations for Inflammatory Bowel Disease: An Ecologic Analysis [J].
Ananthakrishnan, Ashwin N. ;
McGinley, Emily L. ;
Binion, David G. ;
Saeian, Kia .
INFLAMMATORY BOWEL DISEASES, 2011, 17 (05) :1138-1145
[6]
Meta-analysis identifies 29 additional ulcerative colitis risk loci, increasing the number of confirmed associations to 47 [J].
Anderson, Carl A. ;
Boucher, Gabrielle ;
Lees, Charlie W. ;
Franke, Andre ;
D'Amato, Mauro ;
Taylor, Kent D. ;
Lee, James C. ;
Goyette, Philippe ;
Imielinski, Marcin ;
Latiano, Anna ;
Lagace, Caroline ;
Scott, Regan ;
Amininejad, Leila ;
Bumpstead, Suzannah ;
Baidoo, Leonard ;
Baldassano, Robert N. ;
Barclay, Murray ;
Bayless, Theodore M. ;
Brand, Stephan ;
Buening, Carsten ;
Colombel, Jean-Frederic ;
Denson, Lee A. ;
De Vos, Martine ;
Dubinsky, Marla ;
Edwards, Cathryn ;
Ellinghaus, David ;
Fehrmann, Rudolf S. N. ;
Floyd, James A. B. ;
Florin, Timothy ;
Franchimont, Denis ;
Franke, Lude ;
Georges, Michel ;
Glas, Juergen ;
Glazer, Nicole L. ;
Guthery, Stephen L. ;
Haritunians, Talin ;
Hayward, Nicholas K. ;
Hugot, Jean-Pierre ;
Jobin, Gilles ;
Laukens, Debby ;
Lawrance, Ian ;
Lemann, Marc ;
Levine, Arie ;
Libioulle, Cecile ;
Louis, Edouard ;
McGovern, Dermot P. ;
Milla, Monica ;
Montgomery, Grant W. ;
Morley, Katherine I. ;
Mowat, Craig .
NATURE GENETICS, 2011, 43 (03) :246-U94
[7]
Comparison of the fecal microbiota profiles between ulcerative colitis and Crohn's disease using terminal restriction fragment length polymorphism analysis [J].
Andoh, Akira ;
Imaeda, Hirotsugu ;
Aomatsu, Tomoki ;
Inatomi, Osamu ;
Bamba, Shigeki ;
Sasaki, Masaya ;
Saito, Yasuharu ;
Tsujikawa, Tomoyuki ;
Fujiyama, Yoshihide .
JOURNAL OF GASTROENTEROLOGY, 2011, 46 (04) :479-486
[8]
IL-6 promotes immune responses in human ulcerative colitis and induces a skin-homing phenotype in the dendritic cells and Tcells they stimulate [J].
Bernardo, David ;
Vallejo-Diez, Sara ;
Mann, Elizabeth R. ;
Al-Hassi, Hafid O. ;
Martinez-Abad, Beatriz ;
Montalvillo, Enrique ;
Tee, Cheng T. ;
Murugananthan, Aravinth U. ;
Nunez, Henar ;
Peake, Simon T. C. ;
Hart, Ailsa L. ;
Fernandez-Salazar, Luis ;
Garrote, Jose A. ;
Arranz, Eduardo ;
Knight, Stella C. .
EUROPEAN JOURNAL OF IMMUNOLOGY, 2012, 42 (05) :1337-1353
[9]
Inflammatory bowel disease and smoking -: A review of epidemiology, pathophysiology, and therapeutic implications [J].
Birrenbach, T ;
Böcker, U .
INFLAMMATORY BOWEL DISEASES, 2004, 10 (06) :848-859
[10]
Predicting relapse in Crohn's disease: a biopsychosocial model [J].
Bitton, A. ;
Dobkin, P. L. ;
Edwardes, M. D. ;
Sewitch, M. J. ;
Meddings, J. B. ;
Rawal, S. ;
Cohen, A. ;
Vermeire, S. ;
Dufresne, L. ;
Franchimont, D. ;
Wild, G. E. .
GUT, 2008, 57 (10) :1386-1392