FMT for CDI
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB30298 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR2987630_1.fastq.gz | Fastqsanger.gz | |||
| ERR2987630_2.fastq.gz | Fastqsanger.gz | |||
| ERR2987640_1.fastq.gz | Fastqsanger.gz | |||
| ERR2987640_2.fastq.gz | Fastqsanger.gz | |||
| ERR2987650_1.fastq.gz | Fastqsanger.gz |
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Project description:Clostridioides difficile is one of the most common nosocomial pathogens and a global public health threat. Upon colonization of the gastrointestinal tract, C. difficile is exposed to a rapidly changing polymicrobial environment and a dynamic metabolic milieu. Despite the link between the gut microbiota and susceptibility to C. difficile, the impact of synergistic interactions between the microbiota and pathogens on the outcome of infection is largely unknown. Here, we show that microbial cooperation between C. difficile and Enterococcus has a profound impact on the growth, metabolism, and pathogenesis of C. difficile.. Through a process of nutrient restriction and metabolite cross-feeding, E. faecalis shapes the metabolic environment in the gut to enhance C. difficile fitness and increase toxin production. These findings demonstrate that members of the microbiota, such as Enterococcus, have a previously unappreciated impact on C. difficile behavior and virulence.
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Project description:Morphine causes microbial dysbiosis. In this study we focused on restoration of native microbiota in morphine treated mice and looked at the extent of restoration and immunological consequences of this restoration. Fecal transplant has been successfully used clinically, especially for treating C. difficile infection2528. With our expanding knowledge of the central role of microbiome in maintenance of host immune homeostasis17, fecal transplant is gaining importance as a therapy for indications resulting from microbial dysbiosis. There is a major difference between fecal transplant being used for the treatment of C. difficile infection and the conditions described in our studies. The former strategy is based on the argument that microbial dysbiosis caused by disproportionate overgrowth of a pathobiont can be out-competed by re-introducing the missing flora by way of a normal microbiome transplant. This strategy is independent of host factors and systemic effects on the microbial composition. Here, we show that microbial dysbiosis caused due to morphine can be reversed by transplantation of microbiota from the placebo-treated animals.
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Project description:The pathogen Clostridioides difficile causes toxin-mediated diarrhea and is the leading cause of hospital-acquired infection in the United States. Due to growing antibiotic resistance and recurrent infection, targeting C. difficile metabolism presents a new approach to combat this infection. Genome-scale metabolic network reconstructions (GENREs) have been used to identify therapeutic targets and uncover properties that determine cellular behaviors. Thus, we constructed C. difficile GENREs for a hypervirulent isolate (strain [str.] R20291) and a historic strain (str. 630), validating both with in vitro and in vivo data sets. Growth simulations revealed significant correlations with measured carbon source usage (positive predictive value [PPV] ≥ 92.7%), and single-gene deletion analysis showed >89.0% accuracy. Next, we utilized each GENRE to identify metabolic drivers of both sporulation and biofilm formation. Through contextualization of each model using transcriptomes generated from in vitro and infection conditions, we discovered reliance on the pentose phosphate pathway as well as increased usage of cytidine and N-acetylneuraminate when virulence expression is reduced, which was subsequently supported experimentally. Our results highlight the ability of GENREs to identify novel metabolite signals in higher-order phenotypes like bacterial pathogenesis.
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Project description:A major risk factor for Clostridioides difficile infection (CDI) is the perturbation of the gut microbiota by antibiotic administration, and antibiotic therapy, the standard treatment option for CDI, exacerbates the imbalance of the gut microbiota, leading to a very high recurrent CDI (rCDI) incidence rate. Therefore, CDI treatment based on live biotherapeutic products (LBPs) has recently emerged for long-term CDI management and preventive treatment However, there is limited research and understanding of how these LBPs improve CDI symptoms, which raises the need to elucidate the therapeutic mechanisms of LBPs. To fill this knowledge gap, here, we holistically analyzed and investigated the mechanisms involved in the inhibitory effect of probiotics on C. difficile at the molecular level through a multiomics approach on screened strain from probiotics that inhibit C. difficile growth. First, Bifidobacterium species were co-cultured with C. difficile, and B. longum was screened based on its ability to inhibit the growth of C. difficile. Then, the antimicrobial activity of B. longum against C. difficile was confirmed by spot-on-lawn assay and organic acid quantification. Next, we performed proteomic and metabolomic analysis on C. difficile co-cultured with B. longum, and observed physiological changes associated with the inhibition of C. difficile growth and toxin production. It was found that lactate produced by B. longum up-regulated the lactate dehydrogenase complex of C. difficile, leading to a decrease in intracellular ATP synthesis and a subsequent decrease in (deoxy)ribonucleoside triphosphate synthesis. Furthermore, proteinaceous stress induced by B. longum was also identified through the up-regulation of ribosomal proteins, molecular chaperones, and chaperonins, and the down-regulation of translation-related proteins. Finally, we found that B. longum suppressed butyrate metabolism and toxin production by producing and replenishing proline consumed by C. difficile. Therefore, this study will not only expand our understanding of the mechanisms of probiotics' inhibition of C. difficile, but also contribute to the development of LBPs based on molecular mechanisms for treating CDI.
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Project description:16S data from FMT trial for the treatment of recurrent Clostridium difficile infection
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Project description:Recurrent Clostridioides difficile infection (CDI) results in significant morbidity and mortality. We previously established that CDI in mice did not protect against reinfection and was associated with poor pathogen-specific B cell memory (Bmem), recapitulating our observations with human Bmem. Herein, we demonstrate that the secreted toxin TcdB2 is responsible for subversion of Bmem responses. TcdB2 from an endemic C. difficile strain delayed IgG class switch following vaccination, attenuated IgG recall to a vaccine booster, and prevented germinal center formation. The mechanism of TcdB2 action included increased B cell CXCR4 expression and responsiveness to its ligand CXCL12, accounting for altered cell migration and a failure of germinal center-dependent Bmem. These results were reproduced in a C. difficile infection model and an FDA-approved CXCR4-blocking drug rescued germinal center formation. We therefore provide mechanistic insights into C. difficile-associated pathogenesis and illuminate a target for clinical intervention to limit recurrent disease.
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