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Title:
The gut microbiota and inflammatory bowel disease | Seminars in Immunopathology
Description:
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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pubmed, gut, microbiota, article, google, scholar, patients, ibd, disease, cas, colitis, intestinal, bacteria, bowel, ulcerative, central, inflammatory, cells, dysbiosis, inflammation, crohns, remission, reported, mice, genes, mucosal, gastroenterol, observed, bacterial, composition, susceptibility, clinical, fmt, vsl, immune, studies, fecal, nod, essential, treatment, active, trial, cell, paneth, analysis, host, genetic, human, study, epithelial,
Topics {βοΈ}
double-blinded placebo-controlled trials article download pdf germ-free il-10-deficient mice nuclear ribonucleoprotein hnrnp-a1 anti-inflammatory cytokine il-10 adherent-invasive escherichia coli takanori kanai received activity-specific core microbiome serum anti-map antibody mucosal alkaline sphingomyelinase inflammatory bowel disease article matsuoka enabled culture-independent analysis bacterial-derived products tbx21/t-bet t-bet deficiency inflammatory bowel diseases newly diagnosed patients privacy choices/manage cookies genome-wide association study bifidobacterium longum/synergy 1 microbial community imbalances fecal microbiota transplantation microbiota-dependent intestinal inflammation germ-free animals takanori kanai periodically repeated transplantation controlled pilot trial keio university school placebo-controlled trial relapsing inflammatory disorder intestinal microbial ecology randomized controlled trial full access anti-inflammatory effect faecal microbiota transplantation microbial constituents specific distal digestive tract ileo-cecal valves dominant fecal microbiota experimental ulcerative colitis develop spontaneous colitis il-10-deficient mice mucosal barrier function fecal microbiota profiles disease susceptibility genes placebo-controlled study culture-independent analyses cd susceptibility gene developed similar colitis
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- How does dysbiosis lead to intestinal inflammation?
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WebPage:
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headline:The gut microbiota and inflammatory bowel disease
description: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.
datePublished:2014-11-25T00:00:00Z
dateModified:2014-11-25T00:00:00Z
pageStart:47
pageEnd:55
sameAs:https://doi.org/10.1007/s00281-014-0454-4
keywords:
Inflammatory bowel disease
Ulcerative colitis
Crohnβs disease
Dysbiosis
Immunology
Internal Medicine
Pathology
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1863-2300
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headline:The gut microbiota and inflammatory bowel disease
description: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.
datePublished:2014-11-25T00:00:00Z
dateModified:2014-11-25T00:00:00Z
pageStart:47
pageEnd:55
sameAs:https://doi.org/10.1007/s00281-014-0454-4
keywords:
Inflammatory bowel disease
Ulcerative colitis
Crohnβs disease
Dysbiosis
Immunology
Internal Medicine
Pathology
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