TY - JOUR
T1 - The gut microbiota and inflammatory bowel disease
AU - Matsuoka, Katsuyoshi
AU - Kanai, Takanori
N1 - Funding Information:
This study was supported by Grants-in-Aid from the Japanese Ministry of Education, Culture, Sports, Science and Technology; the Health and Labour Sciences Research Grants for Research on Intractable Diseases from the Ministry of Health, Labour and Welfare of Japan; and the Keio University Medical Fund.
Funding Information:
Katsuyoshi Matsuoka received a research grant from Mitsubishi Tanabe Pharma Corporation. Takanori Kanai received a research grant from Mitsubishi Tanabe Pharma Corporation, Eisai Co., Ltd., Abbvie, JIMRO Co., Ltd., Takeda Pharmaceutical Co., Ltd., and ZERIA Co., Ltd.
Publisher Copyright:
© 2014, The Author(s).
PY - 2015/1
Y1 - 2015/1
N2 - 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.
AB - 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.
KW - Crohn’s disease
KW - Dysbiosis
KW - Inflammatory bowel disease
KW - Ulcerative colitis
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U2 - 10.1007/s00281-014-0454-4
DO - 10.1007/s00281-014-0454-4
M3 - Review article
C2 - 25420450
AN - SCOPUS:84925486076
SN - 1863-2297
VL - 37
SP - 47
EP - 55
JO - Seminars in Immunopathology
JF - Seminars in Immunopathology
IS - 1
ER -