Ontology highlight
ABSTRACT:
PROVIDER: PRJNA281490 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1979700_1.fastq.gz | Fastqsanger.gz | |||
| SRR1979700_2.fastq.gz | Fastqsanger.gz | |||
| SRR1979710_1.fastq.gz | Fastqsanger.gz | |||
| SRR1979710_2.fastq.gz | Fastqsanger.gz | |||
| SRR1979720_1.fastq.gz | Fastqsanger.gz |
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Project description:The gut microbiome engenders colonization resistance against the diarrheal pathogen Clostridioides difficile but the molecular basis of this colonization resistance is incompletely understood. A prominent class of gut microbiome-produced metabolites important for colonization resistance against C. difficile is short chain fatty acids (SCFAs). In particular, one SCFA (butyrate) decreases the fitness of C. difficile in vitro and is correlated with C. difficile-inhospitable gut environments, both in mice and in humans. Here, we demonstrate that butyrate-dependent growth inhibition in C. difficile occurs under conditions where C. difficile also produces butyrate as a metabolic end product. Furthermore, we show that exogenous butyrate is internalized into C. difficile cells and is incorporated into intracellular CoA pools where it is metabolized in a reverse (energetically unfavorable) direction to crotonyl-CoA and (S)-3-hydroxybutyryl-CoA and/or 4-hydroxybutyryl-CoA. This internalization of butyrate and reverse metabolic flow of butyrogenic pathway(s) in C. difficile coincides with alterations in toxin release and sporulation. Together, this work highlights butyrate as a marker of a C. difficile inhospitable environment to which C. difficile responds by releasing its diarrheagenic toxins and producing environmentally-resistant spores necessary for transmission between hosts. These findings provide foundational data for understanding the molecular and genetic basis of how C. difficile growth is inhibited by butyrate and how butyrate alters C. difficile virulence in the face of a highly competitive and dynamic gut environment.
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Project description:Analysis of Clostridium difficile (Cd) from the cecal contents of germ-free mice or Bacteroides thetaiotaomicron (Bt)-monocolonized mice on a standard, polysaccharide rich diet or polysaccharide deficient diet 5 days after infection. Results identify genes that are involved in the Cd response to diet, in vivo colonization and in interactions with Bt. In vitro transcriptional profiles of Clostridium difficile obtained from cecal contents of germ-free or Bt-monocolonized mice on a standard, polysaccharide rich or polysaccharide deficient diet. 4 samples/group. 2 control genomic DNA samples for Clostridium difficile and 2 reference genomic DNA samples for Bacteroides thetaiotaomicron Please note that 4 control samples (genomic DNA) were used to determine whether the genomic DNA correctly bound to the probes and thus, were not included in data processing (i.e no processed/normalized data).
2015-08-13 | E-GEOD-60751 | biostudies-arrayexpress
Project description:Toxin A and B from Clostridium difficile are the primary virulence factors in Clostridium difficile disease. The changes in gene transcription of human colon epithelial cells were investigated in vitro in order to better understand the many effects of both toxins.
2012-01-06 | GSE29008 | GEO
Project description:The anaerobic, spore-forming pathogen Clostridioides difficile infects the gastrointestinal tract of higher mammals, including humans, and is the major causative agent of antibiotic-associated diarrhea. Moreover, recurrence and re-infection rates after a first successful antibiotic therapy are substantially high. To overcome the problem of recurrence and re-infection new antibiotics are urgently required that are more selective for the pathogen but spare other members of the microbiota. In turn, the microbial community inside the intestine is allowed to recover and to re-establish colonization resistance to protect against recurrence. The data presented here aim at analyzing the ability of the macrolide compound chlorotonil A to meet the requirements of C. difficile specific drug.
2023-03-29 | PXD029243 | Pride
Project description:We illustrate how metabolically distinct species of Clostridia can protect against or worsen Clostridioides difficile infection, modulating the pathogen's colonization, growth, and virulence to impact host survival. Gnotobiotic mice colonized with the amino acid fermenter Paraclostridium bifermentans survived infection while mice colonized with the butyrate-producer, Clostridium sardiniense, more rapidly succumbed. Systematic in vivo analyses revealed how each commensal altered the gut nutrient environment, modulating the pathogen's metabolism, regulatory networks, and toxin production. Oral administration of P. bifermentans rescued conventional mice from lethal C. difficile infection via mechanisms identified in specifically colonized mice. Our findings lay the foundation for mechanistically informed therapies to counter C. difficile disease using systems biologic approaches to define host-commensal-pathogen interactions in vivo.
2021-10-04 | GSE182613 | GEO
Project description:Clostridium difficile infection (CDI) following antibiotic therapy is a major public health threat. While antibiotic disruption of the indigenous microbiota underlies the majority of cases of CDI, the early dynamics of infection in the disturbed intestinal ecosystem are poorly characterized. This study defines the dynamics of infection with C. difficile strain VPI 10463 throughout the gastrointestinal (GI) tract using a murine model of infection. After inducing susceptibility to C. difficile colonization via antibiotic administration, we followed the dynamics of spore germination, colonization, sporulation, toxin activity, and disease progression throughout the GI tract. C. difficile spores were able to germinate within 6 h postchallenge, resulting in the establishment of vegetative bacteria in the distal GI tract. Spores and cytotoxin activity were detected by 24 h postchallenge, and histopathologic colitis developed by 30 h. Within 36 h, all infected mice succumbed to infection. We correlated the establishment of infection with changes in the microbiota and bile acid profile of the small and large intestines. Antibiotic administration resulted in significant changes to the microbiota in the small and large intestines, as well as a significant shift in the abundance of primary and secondary bile acids. Ex vivo analysis suggested the small intestine as the site of spore germination. This study provides an integrated understanding of the timing and location of the events surrounding C. difficile colonization and identifies potential targets for the development of new therapeutic strategies.
Research is published:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4333439/
2015-06-09 | ST000196 | MetabolomicsWorkbench
Project description:Analysis of Clostridium difficile (Cd) from the cecal contents of germ-free mice or Bacteroides thetaiotaomicron (Bt)-monocolonized mice on a standard, polysaccharide rich diet or polysaccharide deficient diet 5 days after infection. Results identify genes that are involved in the Cd response to diet, in vivo colonization and in interactions with Bt.
2015-08-13 | GSE60751 | GEO
Project description:The Gram-positive bacterium Clostridium difficile, a leading cause of antibiotic-associated pseudomembranous colitis, has received increasing attention due to a rising incidence of clinical C. difficile infections (CDI). Despite progress understanding bacterial factors that promote CDI-associated morbidity and mortality, many fundamental aspects of C. difficile biology remain to be explored. Compared to other Gram-positive pathogens, little is known about the bacterium’s transcriptome architecture and in particular mechanisms of post-transcriptional control. To close this knowledge gap, we have applied a suite of transcriptome-focused techniques, including transcription start site mapping (dRNA-seq), transcription termination mapping, and Hfq RIP-seq, resulting in a single-nucleotide resolution RNA map of C. difficile strain 630.
2021-07-07 | GSE155167 | GEO
Project description:Clostridium difficile is an anaerobic spore-forming rod-shaped gram-positive bacterium that can infect both humans and animals. Most studies on the pathogenesis of C. difficile have focused on its toxins and their effect on the host cells. Recently, we utilized microarrays to identify conserved and divergent genes associated with virulence in C. difficile isolates from humans and animals. Our data provided the first clue toward a complex mechanism underlying host adaptation and pathogenesis. Microarray technology offers an efficient high-throughput tool to study the transcriptional profiles of pathogens and infected host cells. Transcriptomes of C. difficile after exposure to environmental and antibiotic stresses and those of human epithelial colorectal Caco-2 cells upon TcdA treatment have been analyzed. To our knowledge, there are still no reports on the transcriptomic study of host-pathogen interactions for C. difficile infection (CDI). In vitro analyses of interplay between host and pathogen are essential to unravel the mechanisms of infection and to investigate the host response to infection. We therefore employed microarrays to study both bacterial and human cellular transcriptome kinetics during CDI to Caco-2 cells. Here we present a large-scale analysis of transcriptional profiles to reveal molecular determinants playing a role in C. difficile pathogenesis and the host response. We found that there were 254 and 224 differentially-expressed genes after CDI in C. difficile and Caco-2 cells, respectively. These genes are clustered according to their functional categories and their potential roles in pathogenesis and host response are discussed. Our results will not only increase our understanding on the host-pathogen interaction, but may also provide targets for drug development. Clostridium difficile: Control vs Infection (time course) mRNA with genomic DNA of tested and reference strains Caco-2 cells: Control vs Infected with Clostridium difficile Time-course experiments of Caco-2 cells infected with C. difficile for 30, 60 and 120 min
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