Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1179319 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR31146000_1.fastq.gz | Fastqsanger.gz | |||
| SRR31146000_2.fastq.gz | Fastqsanger.gz | |||
| SRR31146001_1.fastq.gz | Fastqsanger.gz | |||
| SRR31146001_2.fastq.gz | Fastqsanger.gz | |||
| SRR31146002_1.fastq.gz | Fastqsanger.gz |
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Project description:Rapidly growing antibiotic resistance among gastrointestinal pathogens, and the ability of antibiotics to induce the virulence of these pathogens makes it increasingly difficult to rely on antibiotics to treat gastrointestinal infections. The probiotic E. coli strain Nissle 1917 (EcN) is the active component of the pharmaceutical preparation Mutaflor® and has been successfully used in the treatment of gastrointestinal disorders. Gut bacteriophages are dominant players in maintaining the microbial homeostasis in the gut, however, their interaction with incoming probiotic bacteria remains to be at conception. The presence of bacteriophages in the gut makes it inevitable for any probiotic bacteria to be phage resistant, in order to survive and successfully colonize the gut. This study addresses the phage resistance of EcN, specifically against lytic T4 phage infection. From various experiments we could show that i) EcN is resistant towards T4 phage infection, ii) EcN’s K5 polysaccharide capsule plays a crucial role in T4 phage resistance and iii) EcN’s lipopolysaccharide (LPS) inactivates T4 phages and notably, treatment with the antibiotic polymyxin B which neutralizes the LPS destroyed the phage inactivation ability of isolated LPS from EcN. Our results further indicate that N-acetylglucosamine at the distal end of O6 antigen in EcN’s LPS could be the interacting partner with T4 phages. From our findings, we have reported for the first time, the role of EcN’s K5 capsule and LPS in its defense against T4 phages. In addition, by inactivating the T4 phages, EcN also protects E. coli K-12 strains from phage infection in tri-culture experiments. The combination of the identified properties is not found in other tested commensal E. coli strains. Furthermore, our research highlights phage resistance as an additional safety feature of EcN, a clinically successful probiotic E. coli strain.
2019-08-27 | GSE135946 | GEO
Project description:MV130 is an inactivated polybacterial mucosal vaccine that confers protection to patients against recurrent respiratory infections, including those of viral etiology. However, its mechanism of action remains poorly understood. Herein, we observe that intranasal prophylaxis with MV130 modulates the lung immune landscape and provides long term heterologous protection against viral respiratory infections in mice. Intranasal administration of MV130 provided protection against systemic candidiasis in wild-type and Rag1-deficient mice lacking functional lymphocytes, indicative of innate immune-mediated protection. Moreover, pharmacological inhibition of trained immunity with metformin abrogated the protection conferred by MV130 against Influenza A virus respiratory infection. MV130 induced reprogramming of mouse bone marrow progenitor cells and human monocytes, promoting an enhanced cytokine production that relied on metabolic and epigenetic shifts. Our results unveil that the mucosal a dministration of a fully inactivated bacterial vaccine provides protection against viral infections by a mechanism associated with the induction of trained immunity. This SuperSeries is composed of the SubSeries listed below.
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Project description:Intergenerational inheritance (Inter-I) of phenotypic characteristics has been demonstrated in plants and invertebrates, with epigenetic modifications playing a role in the inheritance of a variety of features such as appearance1, adaptation to stress, or resistance to infections. Here we provide evidence of Inter-I of transcriptional and epigenetic signatures of trained immunity to the progeny of mice that survived a sublethal systemic Candida albicans infection. Intergenerational trained mice (F1) presented with significant cellular, developmental, transcriptional, and epigenetic changes within the bone marrow resident myeloid effector and progenitor cell compartment. These alterations led to an enhanced responsiveness to in vivo endotoxin challenge and Escherichia coli infection, providing the offspring with protection against heterologous infections. These results argue for the contribution of Lamarckian evolutionary processes to protect against infections in vertebrates.
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Project description:Phage therapy is a promising adjunct therapeutic approach against bacterial multidrug-resistant infections, including Pseudomonas aeruginosa-derived infections. Nevertheless, the current knowledge about the phage-bacteria interaction within a human environment is limited. In this work, we performed a transcriptome analysis of phage-infected P. aeruginosa adhered to a human epithelium (Nuli-1 ATCC® CRL-4011™). To this end, we performed RNA-sequencing from a complex mixture comprising phage–bacteria–human cells at early, middle, and late infection and compared it to uninfected adhered bacteria. Overall, we demonstrated that phage genome transcription is unaltered by bacterial growth and phage employs a core strategy of predation through upregulation of prophage-associated genes, a shutdown of bacterial surface receptors, and motility inhibition. In addition, specific responses were captured under lung-simulating conditions, with the expression of genes related to spermidine syntheses, sulfate acquisition, spermidine syntheses, biofilm formation (both alginate and polysaccharide syntheses), lipopolysaccharide (LPS) modification, pyochelin expression, and downregulation of virulence regulators. These responses should be carefully studied in detail to better discern phage-induced changes from bacterial responses against phage. Our results establish the relevance of using complex settings that mimics in vivo conditions to study phage-bacteria interplay, being obvious the phage versatility on bacterial cell invasion.
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Project description:Enterotoxigenic Escherichia coli (ETEC) infections are a common cause of diarrheal illness in low- and middle-income countries. The live-attenuated ACE527 vaccine, adjuvanted with double mutant LT (dmLT), affords clear but partial protection against ETEC challenge inhuman volunteers. Comparatively, initial wild-type ETEC challenge completely protects against severe diarrhea on homologous re-challenge...To investigate molecular determinants of protection, vaccine antigen content was compared to wild-type ETEC, and proteome microarrays were used to assess immune responses following vaccination and ETEC challenge... Although molecular interrogation of the vaccine confirmed expression of targeted canonical antigens, relative to wild-type ETEC, vaccine strains were deficient in production of flagellar antigens, immotile, and lacked production of the EtpA adhesin. Similarly, vaccination ± dmLT elicited responses to targeted canonical antigens, but relative to wild-type challenge, vaccine responses to some potentially protective non-canonical antigens including EtpA were diminished or absent...These studies highlight important differences in vaccine and wild-type ETEC antigen content and call attention to distinct immunologic signatures that could inform investigation of correlates of protection, and guide vaccine antigen selection for these pathogens of global importance.
2019-07-25 | GSE134792 | GEO
Project description:Ribosome profiling analysis of phage T4 infected E. coli yielded protected mRNA fragments within the normal size range derived from ribosomes stalled at the take-off codon. Ribosomes at this position also yielded some 53 nucleotide fragments, 16 longer. These were due to protection of the nucleotides that form the 5’ stem loop.
2020-06-01 | GSE146240 | GEO
Project description:MV130 is an inactivated polybacterial mucosal vaccine that confers protection to patients against recurrent respiratory infections, including those of viral etiology. We showed that MV130 induces long term heterologous protection against viral respiratory infections in mice. Moreover, intranasal administration of MV130 provided protection against systemic candidiasis in wild-type and Rag1-deficient mice lacking functional lymphocytes, indicative of innate immune-mediated protection. As trained immunity acts via modulation of hematopoietic stem and progenitor cells (Kaufmann et al., 2018; Mitroulis et al., 2018) we hypothesized that MV130 could confer systemic long-term protection through reprogramming of hematopoietic precursors. For that we measured the chromatin accessibility landscape in multipotent progenitors (MPPs) coming from mice treated with MV130 or its excipient using ATAC-seq.
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Project description:Large-genome bacteriophages (jumbo phages) of the Chimalliviriadae family assemble a nucleus-like compartment bounded by a protein shell that protects the replicating phage genome from host-encoded restriction enzymes and CRISPR/Cas nucleases. While the nuclear shell provides broad protection against host nucleases, it necessitates transport of mRNA out of the nucleus-like compartment for translation by host ribosomes, and transport of specific proteins into the nucleus-like compartment to support DNA replication and mRNA transcription. Here we identify a conserved phage nuclear shell-associated protein that we term chimallin C (ChmC), which adopts a nucleic acid-binding fold, binds RNA with high affinity in vitro and binds phage mRNAs in infected cells. ChmC also forms phase-separated condensates with RNA. Targeted knockdown of ChmC using mRNA-targeting Cas13d halts infections at an early stage. Taken together, our data suggest that the conserved ChmC protein acts as a chaperone for phage mRNAs, potentially stabilizing these mRNAs and driving their translocation through the nuclear shell to promote translation and infection progression.
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Project description:The Escherichia coli strain Nissle 1917 (EcN) is used as a probiotic for the treatment of certain gastrointestinal diseases in several European and non-European countries. In vitro studies showed EcN to efficiently inhibit the production of Shiga toxin (Stx) by Stx producing E. coli (STEC) such as Enterohemorrhagic E. coli (EHEC). The occurrence of the latest EHEC serotype (O104:H4) responsible for the great outbreak in 2011 in Germany was due to the infection of an enteroaggregative E. coli by a Stx 2-encoding lambdoid phage turning this E. coli into a lysogenic and subsequently into a Stx producing strain. Since EHEC infected persons are not recommended to be treated with antibiotics, EcN might be an alternative medication. However, because a harmless E. coli strain might be converted into a Stx-producer after becoming host to a stx encoding prophage, we tested EcN for stx-phage genome integration. Our experiments revealed the resistance of EcN towards not only stx-phages but also against the lambda phage. This resistance was not based on the lack of or by mutated phage receptors. Rather the expression of certain genes (superinfection exclusion B (sieB) and a phage repressor (pr) gene) of a defective prophage of EcN was involved in the complete resistance of EcN to infection by the stx- and lambda phage. Obviously, EcN cannot be turned into a Stx producer. Furthermore, we observed EcN to inactivate phages and thereby to protect E. coli K-12 strains against infection by stx- as well as lambda-phages. Inactivation of lambda-phages was due to binding of lambda-phages to LamB of EcN whereas inactivation of stx-phages was caused by a thermostable protein of EcN. These properties together with its ability to inhibit Stx production make EcN a good candidate for the prevention of illness caused by EHEC and probably for the treatment of already infected people.
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