Inflammatory bowel disease: Genetic or environmental diseases?

被引:8
|
作者
Cortot, A. [1 ,2 ]
de Chambrun, G. Pineton [1 ]
Vernier-Massouille, G. [1 ,2 ]
Vigneron, B. [1 ]
Rousseau, C. Gower [2 ]
机构
[1] CHU Lille, Hop Claude Huriez, Serv Hepatogastroenterol, F-59800 Lille, France
[2] CHU Lille, Hop Calmette, INSERM,Serv Epidemiol, InVS,Registre Malad Inflammatoires Chron Intestin, F-59000 Lille, France
来源
GASTROENTEROLOGIE CLINIQUE ET BIOLOGIQUE | 2009年 / 33卷 / 8-9期
关键词
GENOME-WIDE ASSOCIATION; CROHNS-DISEASE; ULCERATIVE-COLITIS; RISK-FACTORS; SUSCEPTIBILITY LOCI; ILEAL MUCOSA; MODERN LIFE; POPULATION; EPIDEMIOLOGY; APPENDECTOMY;
D O I
10.1016/j.gcb.2009.07.005
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Pathophysiology of inflammatory bowel diseases depends on the interaction between genetic susceptibility and environmental factors leading to a deregulated immune intestinal response resulting in bowel lesions. Epidemiologic variations of inflammatory bowel diseases with time (incidence, prevalence) and space suggest a role for risk environmental factors, but so far only smoking habits and appendectomy have been identified as influencing the risk of occurrence and the course of the diseases. Studies of monozygotic and dizygotic twins and the existence of familial aggregation are strong evidence for an important, but not exclusive, role for genetic susceptibility. Since the discovery of NOD2/CARD15 mutations, numerous genes have been associated with inflammatory bowel diseases, some of them involved in the regulation of innate immunity and cellular clearance of infectious agents (autophagy). Thus, new hypothesis include a key role of mucosal human microbiota which could be partly influenced by environmental factors generated by modern life. The improvement of life hygiene, the change of food composition and habits, the industrial pollution in developed countries, may influence, directly or by the way of modifying intestinal human microbiota, inflammatory bowel diseases risk occurrence. (C) 2009 Published by Elsevier Masson SAS.
引用
收藏
页码:681 / 691
页数:11
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