Immunological mechanisms underpinning faecal microbiota transplantation for the treatment of inflammatory bowel disease

被引:48
作者
Quraishi, M. N. [1 ,2 ,3 ]
Shaheen, W. [1 ,3 ]
Oo, Y. H. [1 ,2 ,4 ]
Iqbal, T. H. [1 ,2 ,3 ]
机构
[1] Univ Birmingham, Ctr Liver & Gastroenterol Res, NIHR Birmingham Biomed Res Ctr, Birmingham, W Midlands, England
[2] Univ Hosp Birmingham, Queen Elizabeth Hosp, Dept Gastroenterol, Birmingham, W Midlands, England
[3] Univ Birmingham, Microbiome Treatment Ctr, Birmingham, W Midlands, England
[4] Univ Hosp Birmingham, Queen Elizabeth Hosp, Liver Transplant & Hepatobiliary Unit, Birmingham, W Midlands, England
基金
美国国家卫生研究院;
关键词
faecal microbiota transplantation; immunology; inflammatory bowel disease; REGULATORY T-CELLS; ARYL-HYDROCARBON RECEPTOR; CHAIN FATTY-ACIDS; SEGMENTED FILAMENTOUS BACTERIA; ACTIVE ULCERATIVE-COLITIS; INNATE LYMPHOID-CELLS; CROHNS-DISEASE; GUT MICROBIOTA; INTESTINAL MICROBIOTA; DENDRITIC CELLS;
D O I
10.1111/cei.13397
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Inflammatory bowel disease (IBD) is a chronic gastrointestinal disease that results from a dysregulated immune response against specific environmental triggers in a genetically predisposed individual. Increasing evidence has indicated a causal role for changes in gut microbiota (dysbiosis) contributing to this immune-mediated intestinal inflammation. These mechanisms involve dysregulation of multiple facets of the host immune pathways that are potentially reversible. Faecal microbiota transplantation (FMT) is the transfer of processed stool from a healthy donor into an individual with an illness. FMT has shown promising results in both animal model experiments and clinical studies in IBD in the resolution of intestinal inflammation. The underlying mechanisms, however, are unclear. Insights from these studies have shown interactions between modulation of dysbiosis via changes in abundances of specific members of the gut microbial community and changes in host immunological pathways. Unravelling these causal relationships has promising potential for a translational therapy role to develop targeted microbial therapies and understand the mechanisms that underpin IBD aetiopathogenesis. In this review, we discuss current evidence for the contribution of gut microbiota in the disruption of intestinal immune homeostasis and immunoregulatory mechanisms that are associated with the resolution of inflammation through FMT in IBD.
引用
收藏
页码:24 / 38
页数:15
相关论文
共 129 条
[61]   Glycoantigens Induce Human Peripheral Tr1 Cell Differentiation with Gut-homing Specialization [J].
Kreisman, Lori S. C. ;
Cobb, Brian A. .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2011, 286 (11) :8810-8818
[62]   Variable alterations of the microbiota, without metabolic or immunological change, following faecal microbiota transplantation in patients with chronic pouchitis [J].
Landy, J. ;
Walker, A. W. ;
Li, J. V. ;
Al-Hassi, H. O. ;
Ronde, E. ;
English, N. R. ;
Mann, E. R. ;
Bernardo, D. ;
McLaughlin, S. D. ;
Parkhill, J. ;
Ciclitira, P. J. ;
Clark, S. K. ;
Knight, S. C. ;
Hart, A. L. .
SCIENTIFIC REPORTS, 2015, 5
[63]   Antibiotics in IBD: Still a Role in the Biological Era? [J].
Ledder, Oren ;
Turner, Dan .
INFLAMMATORY BOWEL DISEASES, 2018, 24 (08) :1676-1688
[64]   New IBD genetics: common pathways with other diseases [J].
Lees, C. W. ;
Barrett, J. C. ;
Parkes, M. ;
Satsangi, J. .
GUT, 2011, 60 (12) :1739-1753
[65]   Insights into the role of fecal microbiota transplantation for the treatment of inflammatory bowel disease [J].
Levy, Alexander N. ;
Allegretti, Jessica R. .
THERAPEUTIC ADVANCES IN GASTROENTEROLOGY, 2019, 12
[66]   Fecal microbiota transplantation and bacterial consortium transplantation have comparable effects on the re-establishment of mucosal barrier function in mice with intestinal dysbiosis [J].
Li, Ming ;
Liang, Pin ;
Li, Zhenzhen ;
Wang, Ying ;
Zhang, Guobin ;
Gao, Hongwei ;
Wen, Shu ;
Tang, Li .
FRONTIERS IN MICROBIOLOGY, 2015, 6
[67]   Commensal Clostridia: leading players in the maintenance of gut homeostasis [J].
Lopetuso, Loris R. ;
Scaldaferri, Franco ;
Petito, Valentina ;
Gasbarrini, Antonio .
GUT PATHOGENS, 2013, 5
[68]   Paradoxically Increased FOXP3+T Cells in IBD Do Not Preferentially Express the Isoform of FOXP3 Lacking Exon 2 [J].
Lord, James D. ;
Valliant-Saunders, Karine ;
Hahn, Hejin ;
Thirlby, Richard C. ;
Ziegler, Steven F. .
DIGESTIVE DISEASES AND SCIENCES, 2012, 57 (11) :2846-2855
[69]   Sulfate-reducing bacteria in human feces and their association with inflammatory bowel diseases [J].
Loubinoux, J ;
Bronowicki, JP ;
Pereira, IAC ;
Mougenel, JL ;
Le Faou, AE .
FEMS MICROBIOLOGY ECOLOGY, 2002, 40 (02) :107-112
[70]   Toll-like Receptors and inflammatory Bowel Disease [J].
Lu, Yue ;
Li, Xinrui ;
Liu, Shanshan ;
Zhang, Yifan ;
Zhang, Dekai .
FRONTIERS IN IMMUNOLOGY, 2018, 9