期刊
SEMINARS IN IMMUNOPATHOLOGY
卷 37, 期 1, 页码 47-55出版社
SPRINGER HEIDELBERG
DOI: 10.1007/s00281-014-0454-4
关键词
Inflammatory bowel disease; Ulcerative colitis; Crohn's disease; Dysbiosis
资金
- Japanese Ministry of Education, Culture, Sports, Science and Technology
- Health and Labour Sciences Research Grants for Research on Intractable Diseases from the Ministry of Health, Labour and Welfare of Japan
- Keio University Medical Fund
- Grants-in-Aid for Scientific Research [25460961] Funding Source: KAKEN
Inflammatory bowel disease (IBD) is a chronic and relapsing inflammatory disorder of the gut. Although the precise cause of IBD remains unknown, the most accepted hypothesis of IBD pathogenesis to date is that an aberrant immune response against the gut microbiota is triggered by environmental factors in a genetically susceptible host. The advancement of next-generation sequencing technology has enabled identification of various alterations of the gut microbiota composition in IBD. While some results related to dysbiosis in IBD are different between studies owing to variations of sample type, method of investigation, patient profiles, and medication, the most consistent observation in IBD is reduced bacterial diversity, a decrease of Firmicutes, and an increase of Proteobacteria. It has not yet been established how dysbiosis contributes to intestinal inflammation. Many of the known IBD susceptibility genes are associated with recognition and processing of bacteria, which is consistent with a role of the gut microbiota in the pathogenesis of IBD. A number of trials have shown that therapies correcting dysbiosis, including fecal microbiota transplantation and probiotics, are promising in IBD.
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