scholarly journals Prophage Activation in the Intestine: Insights Into Functions and Possible Applications

2021 ◽  
Vol 12 ◽  
Author(s):  
Jie Hu ◽  
Hao Ye ◽  
Shilan Wang ◽  
Junjun Wang ◽  
Dandan Han

Prophage activation in intestinal environments has been frequently reported to affect host adaptability, pathogen virulence, gut bacterial community composition, and intestinal health. Prophage activation is mostly caused by various stimulators, such as diet, antibiotics, some bacterial metabolites, gastrointestinal transit, inflammatory environment, oxidative stress, and quorum sensing. Moreover, with advancements in biotechnology and the deepening cognition of prophages, prophage activation regulation therapy is currently applied to the treatment of some bacterial intestinal diseases such as Shiga toxin-producing Escherichia coli infection. This review aims to make headway on prophage induction in the intestine, in order to make a better understanding of dynamic changes of prophages, effects of prophage activation on physiological characteristics of bacteria and intestinal health, and subsequently provide guidance on prophage activation regulation therapy.

Food Control ◽  
2018 ◽  
Vol 89 ◽  
pp. 250-259 ◽  
Author(s):  
Brigitte Cadieux ◽  
Anna Colavecchio ◽  
Julie Jeukens ◽  
Luca Freschi ◽  
Jean-Guillaume Emond-Rheault ◽  
...  

2015 ◽  
Vol 215 ◽  
pp. 7-15 ◽  
Author(s):  
Gui-Ying Mei ◽  
Joshua Tang ◽  
Christine Carey ◽  
Susan Bach ◽  
Magdalena Kostrzynska

PLoS ONE ◽  
2017 ◽  
Vol 12 (1) ◽  
pp. e0170050 ◽  
Author(s):  
Rahat Zaheer ◽  
Eric Dugat-Bony ◽  
Devon Holman ◽  
Elodie Cousteix ◽  
Yong Xu ◽  
...  

2016 ◽  
Vol 2016 ◽  
pp. 1-14 ◽  
Author(s):  
Katarzyna Licznerska ◽  
Aleksandra Dydecka ◽  
Sylwia Bloch ◽  
Gracja Topka ◽  
Bożena Nejman-Faleńczyk ◽  
...  

Previous studies indicated that these genetic elements could be involved in the regulation of lysogenization and prophage induction processes. The effects were dramatic in Shiga toxin-converting phageΦ24Bafter treatment with oxidative stress-inducing agent, hydrogen peroxide, while they were less pronounced in bacteriophageλand in both phages irradiated with UV. The hydrogen peroxide-caused prophage induction was found to be RecA-dependent. Importantly, in hydrogen peroxide-treatedE. colicells lysogenic for eitherλorΦ24B, deletion of theexo-xisregion resulted in a significant decrease in the levels of expression of the S.O.S. regulon genes. Moreover, under these conditions, a dramatic decrease in the levels of expression of phage genes crucial for lytic development (particularlyxis, exo, N, cro, O, Q, andR) could be observed inΦ24B-, but not inλ-bearing cells. We conclude that genes located in theexo-xisregion are necessary for efficient expression of both host S.O.S regulon in lysogenic bacteria and regulatory genes of Shiga toxin-converting bacteriophageΦ24B.


2007 ◽  
Vol 190 (1) ◽  
pp. 438-441 ◽  
Author(s):  
Kenan C. Murphy ◽  
Jennifer M. Ritchie ◽  
Matthew K. Waldor ◽  
Anders Løbner-Olesen ◽  
M. G. Marinus

ABSTRACT Shiga toxin 2 (Stx2), one of the principal virulence factors of enterohemorrhagic Escherichia coli, is encoded by 933W, a lambda-like prophage. 933W prophage induction contributes to Stx2 production, and here, we provide evidence that Dam methyltransferase is essential for maintenance of 933W lysogeny. Our findings are consistent with the idea that the 933W prophage has a relatively low threshold for induction, which may promote Stx2 production during infection.


2001 ◽  
Vol 69 (3) ◽  
pp. 1934-1937 ◽  
Author(s):  
Patrick L. Wagner ◽  
David W. K. Acheson ◽  
Matthew K. Waldor

ABSTRACT The Shiga toxins (Stx) are critical virulence factors forEscherichia coli O157:H7 and other serotypes of enterohemorrhagic E. coli (EHEC). These potent toxins are encoded in the genomes of temperate lambdoid bacteriophages. We recently demonstrated that induction of the resident Stx2-encoding prophage in an O157:H7 clinical isolate is required for toxin production by this strain. Since several factors produced by human cells, including hydrogen peroxide (H2O2), are capable of inducing lambdoid prophages, we hypothesized that such molecules might also induce toxin production by EHEC. Here, we studied whether H2O2 and also human neutrophils, an important endogenous source of H2O2, induced Stx2 expression by an EHEC clinical isolate. Both H2O2 and neutrophils were found to augment Stx2 production, raising the possibility that these agents may lead to prophage induction in vivo and thereby contribute to EHEC pathogenesis.


2019 ◽  
Vol 61 (1) ◽  
pp. 131-140 ◽  
Author(s):  
Michalina Filipiak ◽  
Joanna M. Łoś ◽  
Marcin Łoś

AbstractIn the study presented here, we tested, how large a fraction of lysogenic culture was undergoing filamentation, which could indicate triggering of the SOS response or SOS-independent prophage induction that is also known to cause cell filamentation. Here, antibiotic stress was triggered by adding mitomycin C and oxidative stress was induced by hydrogen peroxide. Observation of bacterial cells under an optical microscope revealed more filamenting cells for lysogenic Escherichia coli than for strains not carrying a prophage. Moreover, the amount of filamenting cells depended not only on the stress agents used and the type of the prophage, but also on the host. During induction of the 933W prophage, the resulting phage titer and the amount of elongating cells were different when using E. coli O157:H7 EDL933 clinical isolate and the E. coli MG1655 laboratory strain. The amount of filamenting cells correlates well with the observed phage titers.


2016 ◽  
Vol 2016 ◽  
pp. 1-8 ◽  
Author(s):  
Katarzyna Licznerska ◽  
Bożena Nejman-Faleńczyk ◽  
Sylwia Bloch ◽  
Aleksandra Dydecka ◽  
Gracja Topka ◽  
...  

Virulence of enterohemorrhagicEscherichia coli(EHEC) strains depends on production of Shiga toxins. These toxins are encoded in genomes of lambdoid bacteriophages (Shiga toxin-converting phages), present in EHEC cells as prophages. The genes coding for Shiga toxins are silent in lysogenic bacteria, and prophage induction is necessary for their efficient expression and toxin production. Under laboratory conditions, treatment with UV light or antibiotics interfering with DNA replication are commonly used to induce lambdoid prophages. Since such conditions are unlikely to occur in human intestine, various research groups searched for other factors or agents that might induce Shiga toxin-converting prophages. Among other conditions, it was reported that treatment with H2O2caused induction of these prophages, though with efficiency significantly lower relative to UV-irradiation or mitomycin C treatment. A molecular mechanism of this phenomenon has been proposed. It appears that the oxidative stress represents natural conditions provoking induction of Shiga toxin-converting prophages as a consequence of H2O2excretion by either neutrophils in infected humans or protist predators outside human body. Finally, the recently proposed biological role of Shiga toxin production is described in this paper, and the “bacterial altruism” and “Trojan Horse” hypotheses, which are connected to the oxidative stress, are discussed.


2014 ◽  
Vol 58 (4) ◽  
pp. 2304-2315 ◽  
Author(s):  
Dariusz Nowicki ◽  
Monika Maciąg-Dorszyńska ◽  
Wioletta Kobiela ◽  
Anna Herman-Antosiewicz ◽  
Alicja Węgrzyn ◽  
...  

ABSTRACTThe pathogenicity of enterohemorrhagicEscherichia coli(EHEC) depends on production of Shiga toxins, which are encoded bystxgenes located in the genomes of lambdoid prophages. Efficient expression of these genes requires prophage induction and lytic development of phages. Treatment of EHEC infections is problematic due to not only the resistance of various strains to antibiotics but also the fact that many antibiotics cause prophage induction, thus resulting in high-level expression ofstxgenes. Here we report thatE. coligrowth, Shiga toxin-converting phage development, and production of the toxin by EHEC are strongly inhibited by phenethyl isothiocyanate (PEITC). We demonstrate that PEITC induces the stringent response inE. colithat is mediated by massive production of a global regulator, guanosine tetraphosphate (ppGpp). The stringent response induction arises most probably from interactions of PEITC with amino acids and from amino acid deprivation-mediated activation of ppGpp synthesis. In mutants unable to synthesize ppGpp, development of Shiga toxin-converting phages and production of Shiga toxin are significantly enhanced. Therefore, ppGpp, which appears at high levels in bacterial cells after stimulation of its production by PEITC, is a negative regulator of EHEC virulence and at the same time efficiently inhibits bacterial growth. This is in contrast to stimulation of virulence of different bacteria by this nucleotide reported previously by others.


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