O antigen restricts lysogenization of non-O157 Escherichia coli strains by Stx-converting bacteriophage phi24B

A K Golomidova,A S Kuznetsov,A V Letarov,A D Efimov,I Sh Belalov,E E Kulikov

doi:10.1038/s41598-021-82422-x

A K Golomidova, A S Kuznetsov + Show 4 more

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https://doi.org/10.1038/s41598-021-82422-x

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Journal: Scientific Reports	Publication Date: Feb 4, 2021
Citations: 5	License type: open-access

Affiliation: Lomonosov Moscow State University

Abstract

Acquisition of new prophages that are able to increase the bacterial fitness by the lysogenic conversion is believed to be an important strategy of bacterial adaptation to the changing environment. However, in contrast to the factors determining the range of bacteriophage lytic activity, little is known about the factors that define the lysogenization host range. Bacteriophage phi24B is the paradigmal model of Stx-converting phages, encoding the toxins of the Shiga-toxigenic E. coli (STEC). This virus has been shown to lysogenize a wide range of E. coli strains that is much broader than the range of the strains supporting its lytic growth. Therefore, phages produced by the STEC population colonizing the small or large intestine are potentially able to lysogenize symbiotic E. coli in the hindgut, and these secondary lysogens may contribute to the overall patient toxic load and to lead to the emergence of new pathogenic STEC strains. We demonstrate, however, that O antigen effectively limit the lysogenization of the wild E. coli strains by phi24B phage. The lysogens are formed from the spontaneous rough mutants and therefore have increased sensitivity to other bacteriophages and to the bactericidal activity of the serum if compared to their respective parental strains.

Highlights

Temperate bacteriophages affect many aspects of the life of lysogenic bacteria through multiple mechanisms including direct or indirect influence on the host genome e xpression[1], gene transduction including the recently described highly effective lateral transduction[2] and specific mobilization of some genomic islands[3] and other mechanisms[4]
The majority of STEC strains belong to the O157:H7 s erotype[11], non-O157 STEC strains have been identified and currently gain increased a ttention[4] as, for example, the so-called “Big Six”—O26, O45, O1; O111,O121 and O14512, as well as the O104:H4 serotype that caused the well-known 2011 outbreak in Germany[13]
Toxin expression is repressed in lysogenic bacterial cells, and takes place only upon the prophage induction[15,16]

Summary

Introduction

Temperate bacteriophages affect many aspects of the life of lysogenic bacteria through multiple mechanisms including direct or indirect influence on the host genome e xpression[1], gene transduction including the recently described highly effective lateral transduction[2] and specific mobilization of some genomic islands[3] and other mechanisms[4]. The most known and, probably, the most ecologically significant mechanism of such influence is the lysogenic c onversion[1,5] Such a conversion occurs due to the expression in the lysogen of some prophage encoded genes, that confer the bacteria new features potentially increasing their fitness in particular h abitats[5,6]. The most important factor that determines the bacteriophage host range is not the activity of the intracellular antiviral systems but the specificity of the bacteriophage adsorption. STEC strains possess a number of pathogenicity factors, the foremost being the production of the Shiga toxins[11,14] encoded by the Stx-converting prophages. Many antibiotics increase the induction rate of Stx-converting prophages enhancing the toxin production. The use of antibiotics to treat STEC infections remains c ontroversial[21]

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