Good Gone Bad: One Toxin Away From Disease for Bacteroides fragilis

Valguarnera, Ezequiel; Wardenburg, Juliane Bubeck

doi:10.1016/j.jmb.2019.12.003

Cited by 83 publications

(78 citation statements)

References 239 publications

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“…Bacteroides fragilis, can produce enterotoxins responsible for inflammation and impairment of the intestinal barrier [38]. Conversely, non-toxigenic Bacteroides fragilis exerts beneficial effects by production of short-chain fatty acids and polysaccharide A with anti-inflammatory properties [38]. Prevotella copri, another species belonging to the same phylum, was found to be decreased in psoriasis.…”

Section: Discussionmentioning

confidence: 99%

Gut Microbiome in Psoriasis: An Updated Review

et al. 2020

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(1) Background: A growing body of evidence highlights that intestinal dysbiosis is associated with the development of psoriasis. The gut–skin axis is the novel concept of the interaction between skin diseases and microbiome through inflammatory mediators, metabolites and the intestinal barrier. The objective of this study was to synthesize current data on the gut microbial composition in psoriasis. (2) Methods: We conducted a systematic review of studies investigating intestinal microbiome in psoriasis, using the PRISMA checklist. We searched MEDLINE, EMBASE, and Web of Science databases for relevant published articles (2000–2020). (3) Results: All of the 10 retrieved studies reported alterations in the gut microbiome in patients with psoriasis. Eight studies assessed alpha- and beta-diversity. Four of them reported a lack of change in alpha-diversity, but all confirmed significant changes in beta-diversity. At the phylum-level, at least two or more studies reported a lower relative abundance of Bacteroidetes, and higher Firmicutes in psoriasis patients versus healthy controls. (4) Conclusions: There is a significant association between alterations in gut microbial composition and psoriasis; however, there is high heterogeneity between studies. More unified methodological standards in large-scale studies are needed to understand microbiota’s contribution to psoriasis pathogenesis and its modulation as a potential therapeutic strategy.

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Section: Discussionmentioning

confidence: 99%

Gut Microbiome in Psoriasis: An Updated Review

et al. 2020

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“…Analysis of the "Gratiaviridae" genomes will facilitate the future organization of these families into higher taxonomic ranks, potentially, at the order level. Furthermore, analysis of the "Gratiaviridae" genomes demonstrated the presence of catalase-and DPS-family enzymes that arbitrate cellular responses to oxidative stress [113]. Oxygen concentrations vary along the length of the gastrointestinal tract, where the concentration is lower in the distal vs. proximal gut [114].…”

Section: Discussionmentioning

confidence: 99%

Thousands of Previously Unknown Phages Discovered in Whole-community Human Gut Metagenomes

Benler

Yutin

Antipov

et al. 2020

Preprint

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Background: Double-stranded DNA bacteriophages (dsDNA phages) play pivotal roles in structuring human gut microbiomes; yet, the gut phageome is far from being fully characterized, and additional groups of phages, including highly abundant ones, continue to be discovered by metagenome mining. A multilevel framework for taxonomic classification of viruses was recently adopted, facilitating the classification of phages into evolutionary informative taxonomic units based on hallmark genes. Together with advanced approaches for sequence assembly and powerful methods of sequence analysis, this revised framework offers the opportunity to discover and classify unknown phage taxa in the human gut.Results:A search of human gut metagenomes for circular contigs encoding phage hallmark genes resulted in the identification of 3,738 apparently complete phage genomes that represent 451 putative genera. Several of these phage genera are only distantly related to previously identified phages and are likely to found new families. Two of the candidate families, “Flandersviridae” and “Quimbyviridae”, include some of the most common and abundant members of the human gut virome that infect Bacteroides, Parabacteroides and Prevotella. The third proposed family, “Gratiaviridae”, consists of less abundant phages that are distantly related to the families Autographiviridae, Drexlerviridae and Chaseviridae. Analysis of CRISPR spacers indicates that phages of all three putative families infect bacteria of the phylum Bacteroidetes. Comparative genomic analysis of the three candidate phage families revealed features without precedent in phage genomes. Some “Quimbyviridae” phages possess Diversity-Generating Retroelements (DGRs) that generate hypervariable target genes nested within defense-related genes, whereas the previously known targets of phage-encoded DGRs are structural genes. Several “Flandersviridae” phages encode enzymes of the isoprenoid pathway, a lipid biosynthesis pathway that so far has not been known to be manipulated by phages. The “Gratiaviridae” phages encode a HipA-family protein kinase and glycosyltransferase, suggesting these phages modify the host cell wall, preventing superinfection by other phages. Hundreds of phages in these three and other families are shown to encode catalases and iron-sequestering enzymes that can be predicted to enhance cellular tolerance to reactive oxygen species.Conclusions:Analysis of phage genomes identified in whole-community human gut metagenomes resulted in the delineation of at least three new candidate families of Caudovirales and revealed diverse putative mechanisms underlying phage-host interactions in the human gut. Addition of these phylogenetically classified, diverse and distinct phages to public databases will facilitate taxonomic decomposition and functional characterization of human gut viromes.

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“…Toxigenic Bacteroides fragilis (ETBF) is known to be highly related to several colonic illnesses, including colitis, inflammatory bowel diseases and colon cancers [ 1 , 2 , 3 , 4 ]. The B. fragilis enterotoxin (BFT) is the only virulence factor and is known to be the cause of the above diseases [ 5 , 6 ].…”

Section: Introductionmentioning

confidence: 99%

“…The B. fragilis enterotoxin (BFT) is the only virulence factor and is known to be the cause of the above diseases [ 5 , 6 ]. In addition, BFT-exposed intestinal epithelial cells (IECs) provoke inflammatory signals in the gut [ 1 , 4 , 7 , 8 ]. Although inflammatory signals derived from IECs are observed within the first few hours after exposure to ETBF-derived BFT, little information is available on the signals that control the fate of IECs after the inflammatory signal decreases.…”

Section: Introductionmentioning

confidence: 99%

Bacteroides fragilis Enterotoxin Induces Sulfiredoxin-1 Expression in Intestinal Epithelial Cell Lines Through a Mitogen-Activated Protein Kinases- and Nrf2-Dependent Pathway, Leading to the Suppression of Apoptosis

Jeon

Choi

Lee

et al. 2020

IJMS

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Enterotoxigenic Bacteroides fragilis is a causative agent of colitis and secrets enterotoxin (BFT), leading to the disease. Sulfiredoxin (Srx)-1 serves to protect from oxidative damages. Although BFT can generate reactive oxygen species in intestinal epithelial cells (IECs), no Srx-1 expression has been reported in ETBF infection. In this study, we explored the effects of ETBF-produced BFT on Srx-1 induction in IECs. Treatment of IECs with BFT resulted in increased expression of Srx-1 in a time-dependent manner. BFT treatment also activated transcriptional signals including Nrf2, AP-1 and NF-κB, and the Srx-1 induction was dependent on the activation of Nrf2 signals. Nrf2 activation was assessed using immunoblot and Nrf2-DNA binding activity and the specificity was confirmed by supershift and competition assays. Suppression of NF-κB or AP-1 signals did not affect the upregulation of Srx-1 expression. Nrf2-dependent Srx-1 expression was associated with the activation of p38 mitogen-activated protein kinases (MAPKs) in IECs. Furthermore, suppression of Srx-1 significantly enhanced apoptosis while overexpression of Srx-1 significantly attenuated apoptosis during exposure to BFT. These results imply that a signaling cascade involving p38 and Nrf2 is essential for Srx-1 upregulation in IECs stimulated with BFT. Following this upregulation, Srx-1 may control the apoptosis in BFT-exposed IECs.

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Good Gone Bad: One Toxin Away From Disease for Bacteroides fragilis

Cited by 83 publications

References 239 publications

Gut Microbiome in Psoriasis: An Updated Review

Gut Microbiome in Psoriasis: An Updated Review

Thousands of Previously Unknown Phages Discovered in Whole-community Human Gut Metagenomes

Bacteroides fragilis Enterotoxin Induces Sulfiredoxin-1 Expression in Intestinal Epithelial Cell Lines Through a Mitogen-Activated Protein Kinases- and Nrf2-Dependent Pathway, Leading to the Suppression of Apoptosis

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