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Enhancing phage therapy by coating single bacteriophage-infected bacteria with polymer to preserve phage vitality

ABSTRACT: The efficacy of bacteriophages in treating bacterial infections largely depends on the phages’ vitality, which is impaired when they are naturally released from their hosts, as well as by culture media, manufacturing processes and other insults. Here, by wrapping phage-invaded bacteria individually with a polymeric nanoscale coating to preserve the microenvironment on phage-induced bacterial lysis, we show that, compared with naturally released phages, which have severely degraded proteins in their tail, the vitality of phages isolated from polymer-coated bacteria is maintained. Such latent phages could also be better amplified, and they more efficiently bound and lysed bacteria when clearing bacterial biofilms. In mice with bacterially induced enteritis and associated arthritis, latent phages released from orally administered bacteria coated with a polymer that dissolves at neutral pH had higher bioavailability and led to substantially better therapeutic outcomes than the administration of uncoated phages.

INSTRUMENT(S): LTQ Orbitrap Elite

ORGANISM(S): Salmonella Phage Sfp10

SUBMITTER: Guocheng Xie

LAB HEAD: Jinyao liu

PROVIDER: PXD054755 | Pride | 2025-02-05

REPOSITORIES: pride

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			Action	DRS
	PhageT-1.raw	Raw
	PhageT-2.raw	Raw
	PhageT-3.raw	Raw
	PhageU-1.raw	Raw
	PhageU-2.raw	Raw

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Bacteria conjugate ubiquitin-like proteins to interfere with phage assembly

Project description:Multiple immune pathways in humans conjugate ubiquitin-like proteins to virus and host molecules as a means of antiviral defense. Here we studied an anti-phage defense system in bacteria, comprising a ubiquitin-like protein, ubiquitin-conjugating enzymes E1 and E2, and a deubiquitinase. We show that during phage infection, this system specifically conjugates the ubiquitin-like protein to the phage central tail fiber, a protein at the tip of the tail that is essential for tail assembly as well as for recognition of the target host receptor. Following infection, cells encoding this defense system release a mixture of partially assembled, tailless phage particles, and fully assembled phages in which the central tail fiber is obstructed by the covalently attached ubiquitin-like protein. These phages exhibit severely impaired infectivity, explaining how the defense system protects the bacterial population from the spread of phage infection. Our findings demonstrate that conjugation of ubiquitin-like proteins is an antiviral strategy conserved across the tree of life.

2024-05-08 | GSE262579 | GEO

Influence of the aminoglycoside antibiotic apramycin on host and phage DNA transcription during infection of S. venezuelae ATCC 10712 with phage Alderaan

Project description:Bacterial populations face the constant threat of viral predation exerted by bacteriophages (or phages). In response, bacteria have evolved a wide range of defense mechanisms against phage challenges. Here, we show that aminoglycosides, a well-known class of antibiotics produced by Streptomyces, are potent inhibitors of phage infection. We observed a broad phage inhibition by aminoglycosides. We demonstrate that aminoglycosides do not prevent the injection of phage DNA into bacterial cells but instead block an early step of the viral life cycle. In this context, we used RNA sequencing of S. venezuelae cells infected with phage Alderaan to comparatively investigate the influence of apramycin on phage DNA tanscription at two different time points after inital infection.

2021-04-30 | GSE171784 | GEO

Type I CRISPR-Cas provides robust immunity but incomplete attenuation of phage-induced cellular stress

Project description:During infection, phages manipulate bacteria to redirect metabolism towards viral proliferation. To counteract phages, some bacteria employ CRISPR-Cas systems that provide adaptive immunity. While CRISPR-Cas mechanisms have been studied extensively, their effects on both the phage and the host during phage infection remains poorly understood. Here, we analysed the infection of Serratia by a siphovirus (JS26) and the transcriptomic response with, or without type I-E or I-F CRISPR-Cas immunity. In non-immune Serratia, phage infection altered bacterial metabolism by upregulating anaerobic respiration and amino acid biosynthesis genes, while flagella production was suppressed. Furthermore, phage proliferation required a late-expressed viral Cas4, which did not influence CRISPR adaptation. While type I-E and I-F immunity provided robust defence against phage infection, phage development still impacted the bacterial host. Moreover, DNA repair and SOS response pathways were upregulated during type I immunity. We also discovered that the type I-F system is controlled by a positive autoregulatory feedback loop that is activated upon phage targeting during type I-F immunity, leading to a controlled anti-phage response. Overall, our results provide new insight into phage-host dynamics and the impact of CRISPR immunity within the infected cell.

2021-10-28 | GSE186673 | GEO

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

RIPseq of VP882 phage activation in V. cholerae

Project description:Many, if not all, bacteria use quorum sensing (QS) to control gene expression and collective behaviours, and more recently QS has also been discovered in bacteriophages (phages). Phages can produce communication molecules of their own, or “listen in” on the host’s communication processes, in order to switch between lytic and lysogenic modes of infection. In this project, we studied the interaction of Vibrio cholerae, the causative agent of cholera disease, with the lysogenic vibriophage VP882. The lytic cycle of VP882 is induced by the QS molecule DPO (3,5-dimethylpyrazin-2-ol), however, the global regulatory consequences of DPO-mediated VP882 activation have remained unclear. Using a combination of transcriptomic, genetic, and biochemical approaches, we discovered that induction of VP882 results in binding of phage transcripts to the major RNA chaperone Hfq, which in turn outcompete and down-regulate host-derived Hfq-dependent small RNAs (sRNAs). VP882 itself also encodes Hfq-binding sRNAs and we demonstrate that one of these sRNAs, named VpdS, modulates the expression of multiple host and phage mRNAs through a base-pairing mechanism and thereby promotes phage replication. We further show that host-derived sRNAs can affect phage replication by interfering with the translation of phage mRNAs and thus might be part of the phage defence arsenal of the host. Taken together, our data draw a complex picture of post-transcriptional interactions occurring between host- and phage-derived transcripts that together determine the phage-mediated lysis program.

2023-11-23 | GSE247768 | GEO

RILseq of VP882 phage activation in V. cholerae

2023-11-23 | GSE247767 | GEO

A phage-encoded RNA-binding protein inhibits the antiviral activity of a toxin-antitoxin system

Project description:Bacteria harbor diverse mechanisms to defend themselves against their viral predators, bacteriophages. In response, phages can evolve counter-defense systems, most of which remain poorly understood. In T4-like phages, the gene tifA prevents bacterial defense by the type III toxin-antitoxin (TA) system toxIN, but the mechanism by which TifA inhibits toxIN remains unclear. Here, we show that TifA directly binds both the endoribonuclease ToxN and RNA, leading to the formation of a high molecular weight ribonucleoprotein complex in which ToxN is inhibited. The RNA binding activity of TifA is necessary for its interaction with and inhibition of ToxN. Thus, we propose that TifA inhibits ToxN during phage infection by trapping ToxN on cellular RNA, particularly the abundant 16S rRNA, preventing cleavage of phage transcripts. Taken together, our results reveal a novel mechanism underlying inhibition of a phage-defensive RNase toxin by a small, phage-encoded protein.

2023-12-04 | GSE234211 | GEO

Investigating Lactococcus lactis MG1363 response to phage p2 infection at the proteome level

Project description:Phages are viruses that specifically infect and kill bacteria. Bacterial fermentation and biotechnology industries see them as enemies, however, they are also investigated for the treatment or prevention of infections caused by multidrug resistant bacteria. Whether foes or allies, their importance is undeniable. Despite decades of research some aspects of phage biology are still poorly understood. In this study, we used label-free quantitative proteomics to reveal the proteotypes of Lactococcus lactis MG1363 during infection by the virulent phage p2, a model for studying the biology of phages infecting Gram-positive bacteria. Our approach resulted in the high-confidence detection and quantification of 59% of the theoretical bacterial proteome, including 226 bacterial proteins detected only during phage infection and 6 proteins unique to uninfected bacteria. We also identified many bacterial proteins of differing abundance during the infection. Using this high-throughput proteomic datasets, we selected specific bacterial genes for inactivation using CRISPR-Cas9 to investigate their involvement in phage replication. One knockout mutant lacking gene llmg_0219 showed resistance to phage p2 due to a deficiency in phage adsorption. Furthermore, we detected and quantified 78% of the theoretical phage proteome and identified many proteins of phage p2 that had not been previously detected. Among others, we uncovered a conserved small phage protein (ORFN1) coded by an unannotated gene. We also applied a targeted approach to achieve greater sensitivity and identify undetected phage proteins that were expected to be present. This allowed us to follow the fate of ORF46, a small phage protein of low abundance. In summary, this work offers a unique view of the virulent phages’ takeover of bacterial cells and provides novel information on phage-host interactions.

2019-01-29 | PXD011263 | Pride

RNAseq of VP882 and VP882 ∆vpdS phage activation in V. cholerae

2023-11-23 | GSE247769 | GEO

Phage-Antibiotic Combinations Against Klebsiella pneumoniae

Project description:hvKP ATCC43816 and its lytic phage H5 were employed as a phage-antibiotic combination model. Based on the comprehensive characterization of phages, including cryo-electron microscopy, we evaluated the synergic effect of H5 on bacterial killing in vitro when combined with multiple antibiotics, and analyzed the advantages of phage-antibiotic combinations from an evolutionary perspective and proposes a novel PAS mechanism by using ceftazidime as an example.

2023-09-14 | GSE237490 | GEO

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