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      Colicin F Y inhibits pathogenic Yersinia enterocolitica in mice

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          Abstract

          Yersiniosis belongs to the common foodborne diseases around the world, and frequently manifests as diarrhea that can be treated with probiotics. Colicin F Y is an antibacterial agent produced by bacteria and it is capable of specific growth inhibition of Yersinia enterocolitica, the causative agent of gastrointestinal yersiniosis. In this study, recombinant E. coli producing colicin F Y were constructed, using both known probiotic strains EcH22 and EcColinfant, and the newly isolated murine strains Ec1127 and Ec1145. All E. coli strains producing colicin F Y inhibited growth of pathogenic Y. enterocolitica during co-cultivation in vitro. In dysbiotic mice treated with streptomycin, E. coli strains producing colicin F Y inhibited progression of Y. enterocolitica infections. This growth inhibition was not observed in mice with normal gut microflora, likely due to insufficient colonization capacity of E. coli strains and/or due to spatial differences in intestinal niches. Isogenic Y. enterocolitica producing colicin F Y was constructed and shown to inhibit pathogenic Y. enterocolitica in mice with normal microflora. Evidence of in vivo antimicrobial activity of colicin F Y may have utility in the treatment of Y. enterocolitica infections.

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          Colicin biology.

          Colicins are proteins produced by and toxic for some strains of Escherichia coli. They are produced by strains of E. coli carrying a colicinogenic plasmid that bears the genetic determinants for colicin synthesis, immunity, and release. Insights gained into each fundamental aspect of their biology are presented: their synthesis, which is under SOS regulation; their release into the extracellular medium, which involves the colicin lysis protein; and their uptake mechanisms and modes of action. Colicins are organized into three domains, each one involved in a different step of the process of killing sensitive bacteria. The structures of some colicins are known at the atomic level and are discussed. Colicins exert their lethal action by first binding to specific receptors, which are outer membrane proteins used for the entry of specific nutrients. They are then translocated through the outer membrane and transit through the periplasm by either the Tol or the TonB system. The components of each system are known, and their implication in the functioning of the system is described. Colicins then reach their lethal target and act either by forming a voltage-dependent channel into the inner membrane or by using their endonuclease activity on DNA, rRNA, or tRNA. The mechanisms of inhibition by specific and cognate immunity proteins are presented. Finally, the use of colicins as laboratory or biotechnological tools and their mode of evolution are discussed.
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            Bacteriocins: evolution, ecology, and application.

            Microbes produce an extraordinary array of microbial defense systems. These include classical antibiotics, metabolic by-products, lytic agents, numerous types of protein exotoxins, and bacteriocins. The abundance and diversity of this potent arsenal of weapons are clear. Less clear are their evolutionary origins and the role they play in mediating microbial interactions. The goal of this review is to explore what we know about the evolution and ecology of the most abundant and diverse family of microbial defense systems: the bacteriocins. We summarize current knowledge of how such extraordinary protein diversity arose and is maintained in microbial populations and what role these toxins play in mediating microbial population-level and community-level dynamics. In the latter half of this review we focus on the potential role bacteriocins may play in addressing human health concerns and the current role they serve in food preservation.
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              Bacteriocin production as a mechanism for the antiinfective activity of Lactobacillus salivarius UCC118.

              The mechanisms by which probiotic strains enhance the health of the host remain largely uncharacterized. Here we demonstrate that Lactobacillus salivarius UCC118, a recently sequenced and genetically tractable probiotic strain of human origin, produces a bacteriocin in vivo that can significantly protect mice against infection with the invasive foodborne pathogen Listeria monocytogenes. A stable mutant of Lb. salivarius UCC118 that is unable to produce the Abp118 bacteriocin also failed to protect mice against infection with two strains of L. monocytogenes, EGDe and LO28, confirming that bacteriocin production is the primary mediator of protection against this organism. Furthermore, Lb. salivarius UCC118 did not offer any protection when mice were infected with a strain of L. monocytogenes expressing the cognate Abp118 immunity protein AbpIM, confirming that the antimicrobial effect is a result of direct antagonism between Lb. salivarius and the pathogen, mediated by the bacteriocin Abp118.
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                Author and article information

                Contributors
                dsmajs@med.muni.cz
                Journal
                Sci Rep
                Sci Rep
                Scientific Reports
                Nature Publishing Group UK (London )
                2045-2322
                16 August 2018
                16 August 2018
                2018
                : 8
                : 12242
                Affiliations
                [1 ]ISNI 0000 0001 2194 0956, GRID grid.10267.32, Department of Biology, Faculty of Medicine, , Masaryk University, ; Brno, Czech Republic
                [2 ]ISNI 0000 0001 2194 0956, GRID grid.10267.32, Research Centre for Toxic Compounds in the Environment, Faculty of Science, , Masaryk University, ; Brno, Czech Republic
                [3 ]ISNI 0000 0001 2285 286X, GRID grid.426567.4, Veterinary Research Institute, ; Brno, Czech Republic
                Article
                30729
                10.1038/s41598-018-30729-7
                6095899
                30115964
                ce569f38-db08-495d-bd93-746d2fe1dc87
                © The Author(s) 2018

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

                History
                : 3 May 2018
                : 6 August 2018
                Funding
                Funded by: National Program of Sustainability: LO1218
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