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      Microbial competition between Escherichia coli and Candida albicans reveals a soluble fungicidal factor

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          Abstract

          Localized and systemic fungal infections caused by Candida albicans can lead to significant mortality and morbidity. However, severe C. albicans infections are relatively rare, occurring mostly in the very young, the very old, and immunocompromised individuals. The fact that these infections are rare is interesting because as much as 80 percent of the population is asymptomatically colonized with C. albicans. It is thought that members of the human microbiota and the immune system work in concert to reduce C. albicans overgrowth through competition and modification of the growth environment. Here, we report that Escherichia coli (strain MG1655) outcompetes and kills C. albicans (strain SC5314) in vitro. We find that E. coli produces a soluble factor that kills C. albicans in a magnesium-dependent fashion such that depletion of available magnesium is essential for toxicity.

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          Most cited references34

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          Medically important bacterial-fungal interactions.

          Whether it is in the setting of disease or in a healthy state, the human body contains a diverse range of microorganisms, including bacteria and fungi. The interactions between these taxonomically diverse microorganisms are highly dynamic and dependent on a multitude of microorganism and host factors. Human disease can develop from an imbalance between commensal bacteria and fungi or from invasion of particular host niches by opportunistic bacterial and fungal pathogens. This Review describes the clinical and molecular characteristics of bacterial-fungal interactions that are relevant to human disease.
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            Bacteriocin production augments niche competition by enterococci in the mammalian GI tract

            Enterococcus faecalis (EF) is both a common commensal of the human gastrointestinal tract (GI) and a leading cause of hospital acquired infections 1 . Systemic infections with multi-drug resistant enterococci occur subsequent to GI colonization 2 . Preventing colonization by multi-drug resistant EF could therefore be a valuable approach to limiting infection. However, little is known about mechanisms EF uses to colonize and compete for stable gastrointestinal niches. Pheromone-responsive, conjugative plasmids encoding bacteriocins are common among enterococcal strains 3 , and could modulate niche competition among enterococci or between enterococci and the intestinal microbiota. We developed a model of mouse gut colonization with EF without disrupting the microbiota, to evaluate the role of the conjugative plasmid pPD1 expressing bacteriocin 21 4 on enterococcal colonization. Here we show that EF harboring pPD1 replaces indigenous enterococci and outcompetes EF lacking pPD1. Furthermore, in the intestine, pPD1 is transferred to other EF strains by conjugation, enhancing their survival. Moreover, colonization with an EF strain carrying a conjugation-defective pPD1 mutant resulted in clearance of vancomycin-resistant enterococci, without plasmid transfer. Therefore bacteriocin expression by commensal bacteria can influence niche-competition in the GI tract, and bacteriocins, delivered by commensals that occupy a precise intestinal bacterial niche, may be an effective therapeutic approach to specifically eliminate intestinal colonization by multi-drug resistant bacteria, without profound disruption of the indigenous microbiota.
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              The role of lactic acid production by probiotic Lactobacillus species in vaginal health

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                Author and article information

                Journal
                Microb Cell
                Microb Cell
                Microb Cell
                Microb Cell
                Microbial Cell
                Shared Science Publishers OG
                2311-2638
                07 March 2018
                07 May 2018
                : 5
                : 5
                : 249-255
                Affiliations
                [1 ]Department of Molecular Microbiology and Immunology, Division of Biology and Medicine, Brown University, Providence, RI, 02912, USA.
                [2 ]Bryant University, Smithfield, RI, 02917 USA.
                [3 ]Universidad Autónoma de Nuevo León, Facultad de Ciencias Químicas, Pedro de Alba, S/N, San Nicolás de los Garza, Nuevo León, México.
                [4 ]Centro de Investigacion en Biotecnologia y Nanotecnologia, Universidad Autonoma de Nuevo Leon, Facultad de Ciencias Quimicas, Parque de Investigacion e Innovacion Tecnologica, Km. 10 autopista al Aeropuerto Internacional Mariano Escobedo, Apodaca, Nuevo Leon. 66629.
                Author notes

                Conflict of interest: The authors have no conflicts of interest to report.

                Please cite this article as: Damien J. Cabral, Swathi Penumutchu, Colby Norris, Ruben Morones-Ramirez and Peter Belenky ( 2018). Microbial competition between Escherichia coli and Candida albicans reveals a soluble fungicidal factor. Microbial Cell 5(5): 249-255. doi: 10.15698/mic2018.05.631

                Article
                MIC0177E180
                10.15698/mic2018.05.631
                5961918
                29796389
                1b96725a-fef7-4f2f-b4f5-18bbc070a9fe
                Copyright @ 2018

                This is an open-access article released under the terms of the Creative Commons Attribution (CC BY) license, which allows the unrestricted use, distribution, and reproduction in any medium, provided the original author and source are acknowledged.

                History
                : 15 December 2017
                : 22 February 2018
                Funding
                This work was supported by grant number P20GM103430 from the National Institute of General Medical Sciences of the National Institutes of Health through the IDeA Network of Biomedical Research (INBRE) program and by the basic science grant 221332 from CONACyT. Additional support was provided by grants from the National Science Foundation Graduate Research Fellowship (Grant No. 1644760) and the Center for Computational Biology of Human Disease (NIH P20 GM109035). Finally, additional funding was provided by the Paicyt 2016-2017 Science Grant from the Universidad Autónoma de Nuevo León and the Fronteras de la Ciencia grant 1502 and Infraestructura Grant 279957 from CONACyT. We would also like to thank Dr. James Collins (Massachusetts Institute of Technology) for his guidance and advice on this project.
                Categories
                Microbiology
                Applied Microbiology
                Molecular Biology
                Genetics

                microbial competition,escherichia coli,candida albicans,antifungal,magnesium

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