The Microbiota in Inflammatory Bowel Disease

A special issue of Microorganisms (ISSN 2076-2607). This special issue belongs to the section "Gut Microbiota".

Deadline for manuscript submissions: closed (31 August 2021) | Viewed by 5485

Special Issue Editor


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Guest Editor
Department of Gastroenterology, Copenhagen University Hospital Hvidovre, 2650 Hvidovre, Denmark
Interests: inflammatory bowel diseases; intestinal dysbiosis; fecal microbiota transplantation; probiotics

Special Issue Information

Dear Colleagues,

Modulation of the gut microbiota using fecal microbiota transplantation (FMT), diet or pre-, pro-, or antibiotics is attracting increased attention as potential future treatment modalities for a wide range of intestinal dysbiosis-related diseases, including inflammatory bowel disease (IBD), irritable bowel syndrome (IBS), antibiotic-associated diarrhea, obesity, intestinal cancer, and more. A substantial imbalance has been observed across major bacterial phyla, including Firmicutes, Bacteroidetes, Proteobacteria and Actinobacteria, influencing the intestinal microbiomes’ beneficial effects on the host through changes in the production of short-chain fatty acids (SCFA) and amino acids, metabolism of undigested carbohydrate, and stimulation of the immune system. Recent publications have demonstrated positive effects of FMT on disease activity in IBD in randomized placebo-controlled trials. Furthermore, abundance or lack of a single or a few bacterial species such as, e.g., Faecalibacterium Prausnitzii and E. coli pathobionts, could possibly be decisive in disease outcome. Therefore, precision modulation of the intestinal microbiome may be a viable principle for a targeted future treatment of IBD, with few side effects. We welcome original research articles or review articles on all kinds of microbiota manipulation in IBD, focusing on clinical outcomes in vitro, in animal and in human studies.

Dr. Andreas Munk Petersen
Guest Editor

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Keywords

  • Inflammatory bowel disease
  • Ulcerative colitis
  • Crohn’s disease
  • Microbiota
  • Probiotics
  • Fecal microbiota transplantation
  • Antibiotics
  • Dysbiosis

Published Papers (2 papers)

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Research

12 pages, 2472 KiB  
Article
Alleviative Effects of Exopolysaccharide Produced by Lactobacillus helveticus KLDS1.8701 on Dextran Sulfate Sodium-Induced Colitis in Mice
by Yin Liu, Shujuan Zheng, Jiale Cui, Tingting Guo, Jingtao Zhang and Bailiang Li
Microorganisms 2021, 9(10), 2086; https://doi.org/10.3390/microorganisms9102086 - 2 Oct 2021
Cited by 18 | Viewed by 2125
Abstract
Ulcerative colitis (UC) is a non-specific chronic inflammatory disease with lesions located in the colon and rectum. The aim of this study was to evaluate the anti-inflammatory effects of exopolysaccharide-1 (EPS-1) isolated by L. helveticus KLDS1.8701 on UC. The anti-inflammatory effects of EPS-1 [...] Read more.
Ulcerative colitis (UC) is a non-specific chronic inflammatory disease with lesions located in the colon and rectum. The aim of this study was to evaluate the anti-inflammatory effects of exopolysaccharide-1 (EPS-1) isolated by L. helveticus KLDS1.8701 on UC. The anti-inflammatory effects of EPS-1 were studied using dextran sulphate sodium (DSS)-induced UC model. In vivo results showed that EPS-1 administration significantly ameliorated weight loss, colon shortening, disease activity index (DAI) score, myeloperoxidase (MPO) activity, and colon tissue damage. In addition, EPS-1 administration significantly decreased the levels of pro-inflammatory cytokines and increased levels of anti-inflammatory cytokines. Meanwhile, EPS-1 administration significantly up-regulated the expression of tight junction proteins and mucin. Furthermore, EPS-1 administration modulated gut microbiota composition caused by DSS and increased the short-chain fatty acids (SCFAs) levels. Collectively, our study showed the alleviative effects of EPS- isolated by L. helveticus KLDS1.8701 on DSS-induced UC via alleviating intestinal inflammation, improving mucosal barrier function, and modulating gut microbiota composition. Full article
(This article belongs to the Special Issue The Microbiota in Inflammatory Bowel Disease)
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12 pages, 1159 KiB  
Article
Modulation of the Mucosa-Associated Microbiome Linked to the PTPN2 Risk Gene in Patients with Primary Sclerosing Cholangitis and Ulcerative Colitis
by Luisa Denoth, Pascal Juillerat, Andreas E. Kremer, Gerhard Rogler, Michael Scharl, Bahtiyar Yilmaz, Sena Bluemel and on behalf of the Swiss IBD Cohort Study
Microorganisms 2021, 9(8), 1752; https://doi.org/10.3390/microorganisms9081752 - 17 Aug 2021
Cited by 6 | Viewed by 2567
Abstract
Gut microbiota appears to be involved in the pathogenesis of primary sclerosing cholangitis (PSC). The protein tyrosine phosphatase nonreceptor 2 (PTPN2) gene risk variant rs1893217 is associated with gut dysbiosis in inflammatory bowel disease (IBD), and PTPN2 was mentioned as a possible risk [...] Read more.
Gut microbiota appears to be involved in the pathogenesis of primary sclerosing cholangitis (PSC). The protein tyrosine phosphatase nonreceptor 2 (PTPN2) gene risk variant rs1893217 is associated with gut dysbiosis in inflammatory bowel disease (IBD), and PTPN2 was mentioned as a possible risk gene for PSC. This study assessed the microbial profile of ulcerative colitis (UC) patients with PSC and without PSC (non-PSC). Additionally, effects of the PTPN2 risk variant were assessed. In total, 216 mucosal samples from ileum, colon, and rectum were collected from 7 PSC and 42 non-PSC patients, as well as 28 control subjects (non-IBD). The microbial composition was derived from 16S rRNA sequencing data. Overall, bacterial richness was highest in PSC patients, who also had a higher relative abundance of the genus Roseburia compared to non-PSC, as well as Haemophilus, Fusobacterium, Bifidobacterium, and Actinobacillus compared to non-IBD, as well as a lower relative abundance of Bacteroides compared to non-PSC and non-IBD, respectively. After exclusion of patients with the PTPN2 risk variant, Brachyspira was higher in PSC compared to non-PSC, while, solely in colon samples, Eubacterium and Tepidimonas were higher in PSC vs. non-IBD. In conclusion, this study underlines the presence of gut mucosa-associated microbiome changes in PSC patients and rather weakens the role of PTPN2 as a PSC risk gene. Full article
(This article belongs to the Special Issue The Microbiota in Inflammatory Bowel Disease)
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