The Anti-inflammatory Immune Regulation Induced by Butyrate Is Impaired in Inflamed Intestinal Mucosa from Patients with Ulcerative Colitis
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Title
The Anti-inflammatory Immune Regulation Induced by Butyrate Is Impaired in Inflamed Intestinal Mucosa from Patients with Ulcerative Colitis
Authors
Keywords
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Journal
INFLAMMATION
Volume -, Issue -, Pages -
Publisher
Springer Science and Business Media LLC
Online
2019-12-03
DOI
10.1007/s10753-019-01133-8
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Note: Only part of the references are listed.- Effect of Fecal Microbiota Transplantation on 8-Week Remission in Patients With Ulcerative Colitis
- (2019) Samuel P. Costello et al. JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
- Butyrate does not protect against inflammation-induced loss of epithelial barrier function and cytokine production in primary cell monolayers from patients with ulcerative colitis
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- (2019) Georgios Mavroudis et al. Journal of Crohns & Colitis
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- Microbial shifts and signatures of long-term remission in ulcerative colitis after faecal microbiota transplantation
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- Butyrate and propionate inhibit antigen-specific CD8+ T cell activation by suppressing IL-12 production by antigen-presenting cells
- (2017) Claudia Nastasi et al. Scientific Reports
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- (2017) Hui Yan et al. PLoS One
- Butyrate-producing bacteria supplemented in vitro to Crohn’s disease patient microbiota increased butyrate production and enhanced intestinal epithelial barrier integrity
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- Butyrate inhibits interleukin-17 and generates Tregs to ameliorate colorectal colitis in rats
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- A decrease of the butyrate-producing speciesRoseburia hominisandFaecalibacterium prausnitziidefines dysbiosis in patients with ulcerative colitis
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- Commensal microbe-derived butyrate induces the differentiation of colonic regulatory T cells
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- Butyrate interferes with the differentiation and function of human monocyte-derived dendritic cells
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- Butyrate Attenuates Lipopolysaccharide-Induced Inflammation in Intestinal Cells and Crohn's Mucosa through Modulation of Antioxidant Defense Machinery
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- Impaired butyrate oxidation in ulcerative colitis is due to decreased butyrate uptake and a defect in the oxidation pathway*
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- The dietary histone deacetylase inhibitor sulforaphane induces human β-defensin-2 in intestinal epithelial cells
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