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K5 capsule and lipopolysaccharide are important in resistance to T4 phage attack in probiotic E. coli strain Nissle 1917

ABSTRACT: K5 capsule and lipopolysaccharide are important in resistance to T4 phage attack in probiotic E. coli strain Nissle 1917

PROVIDER: PRJNA560715 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9994130.fastq.gz	Fastqsanger.gz
	SRR9994131.fastq.gz	Fastqsanger.gz
	SRR9994132.fastq.gz	Fastqsanger.gz
	SRR9994133.fastq.gz	Fastqsanger.gz
	SRR9994134.fastq.gz	Fastqsanger.gz

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K5 capsule and lipopolysaccharide are important in resistance to T4 phage attack in probiotic E. coli strain Nissle 1917

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

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Project description:Confluent Caco-2 cells cultured over 6 hours non-treated with E.coli Nissle 1917 (GSM40938 and GSM40941). Confluent Caco-2 cells cocultured over 6 hours with E.coli Nissle 1917 (GSM40881 and GSM40937). Keywords: parallel sample

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Transcription profiling of human Caco-2 cells cocultured with E.coli Nissle 1917

Project description:Confluent Caco-2 cells cultured over 6 hours non-treated with E.coli Nissle 1917; (GSM40938 and GSM40941). Confluent Caco-2 cells cocultured over 6 hours with E.coli Nissle 1917 (GSM40881 and GSM40937).

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Escherichia coli Nissle 1917

Project description:Draft Genome Sequence of Escherichia coli Strain Nissle 1917 (serovar O6:K5:H1)

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E. coli Nissle 1917 transcriptional response after treatment with Calprotectin

Project description:To determine whether calprotectin can elicit any transcriptional response in the probiotic E. coli Nissle 1917(EcN), EcN was treated with 200 ug/g of calprotectin in log phase.

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K5 Capsule and Lipopolysaccharide Are Important in Resistance to T4 Phage Attack in Probiotic <i>E. coli</i> Strain Nissle 1917.

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 Escherichia 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 toward 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. Combination of these identified properties in EcN was not found in other tested commensal E. coli strains. Our results further indicated 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. Our research highlights phage resistance as an additional safety feature of EcN, a clinically successful probiotic E. coli strain.

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RNA sequencing of Escherichia coli Nissle 1917 after HOCl stress

Project description:RNA sequencing of Escherichia coli Nissle 1917 before and after HOCl treatment was perfomed to identify pathways that may be important in responding to oxidative stress caused by reachive chlorine species (RCS).

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Comparative genomic hybridization by array of E. coli strains CFT073, Nissle 1917 and ABU 83872

Project description:CGH analysis of CFT073, Nissle 1917 and ABU 83972

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Project description:Escherichia coli Nissle 1917 Genome sequencing

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