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  • 1
    Online Resource
    Online Resource
    Microbiology Society ; 2020
    In:  Microbiology Vol. 166, No. 11 ( 2020-12-01), p. 1038-1046
    In: Microbiology, Microbiology Society, Vol. 166, No. 11 ( 2020-12-01), p. 1038-1046
    Abstract: Vibrio cholerae, the aetiological agent of cholera, possesses multiple iron acquisition systems, including those for the transport of siderophores. How these systems benefit V. cholerae in low-iron, polymicrobial communities in environmental settings or during infection remains poorly understood. Here, we demonstrate that in iron-limiting conditions, co-culture of V. cholerae with a number of individual siderophore-producing microbes significantly promoted V. cholerae growth in vitro . We further show that in the host environment with low iron, V. cholerae colonizes better in adult mice in the presence of the siderophore-producing commensal Escherichia coli . Taken together, our results suggest that in aquatic reservoirs or during infection, V. cholerae may overcome environmental and host iron restriction by hijacking siderophores from other microbes.
    Type of Medium: Online Resource
    ISSN: 1350-0872 , 1465-2080
    Language: English
    Publisher: Microbiology Society
    Publication Date: 2020
    detail.hit.zdb_id: 2008736-6
    SSG: 12
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  • 2
    Online Resource
    Online Resource
    American Society for Microbiology ; 2021
    In:  Applied and Environmental Microbiology Vol. 87, No. 18 ( 2021-08-26)
    In: Applied and Environmental Microbiology, American Society for Microbiology, Vol. 87, No. 18 ( 2021-08-26)
    Abstract: Biofilm formation is important in both the environmental and intestinal phases of the Vibrio cholerae life cycle. Nevertheless, most studies of V. cholerae biofilm formation focus on monospecies cultures, whereas nearly all biofilm communities found in nature consist of a variety of microorganisms. Multispecies biofilms formed between V. cholerae and other bacteria in the environment and the interactions that exist between these species are still poorly understood. In this study, the influence of Escherichia coli on the biofilm formation of V. cholerae was studied in the context of both in vitro coculture and in vivo coinfection. To understand the underlying synergistic mechanisms between these two species and to investigate the role of E. coli in V. cholerae biofilm formation, different pathotypes of E. coli and corresponding deletion mutants lacking genes that influence flagellar motility, curli fibers, or type I pili were cocultured with V. cholerae . Our findings demonstrate that the presence of commensal E. coli increases biofilm formation at the air-liquid interface in vitro and the generation of biofilm-like multicellular clumps in mouse feces. Examination of laboratory E. coli flagellar-motility Δ fliC and Δ motA mutants in dual-species biofilm formation suggests that flagellar motility plays an important role in the synergistic interaction and coaggregation formation between V. cholerae and E. coli . This study facilitates a better understanding of how V. cholerae resides in harsh environments and colonizes the intestine. IMPORTANCE Biofilms play an important role in the V. cholerae life cycle. Until now, only monospecies biofilm formation of V. cholerae has been well studied. However, in nature, bacteria live in complex microbial communities, where biofilm is mostly composed of multiple microbial species that interact to cooperate with or compete against each other. Uncovering how V. cholerae forms multispecies biofilms is critical for furthering our understanding of how V. cholerae survives in the environment and transitions to infecting the human host. In this work, the dual-species biofilm containing V. cholerae and Escherichia coli was investigated. We demonstrate that the presence of commensal E. coli increased overall biofilm formation. Furthermore, we demonstrate that the motility of E. coli flagella is important for V. cholerae and E. coli to form coaggregation clumps in a dual-species biofilm. These results shed light on a new mechanism for understanding the survival and pathogenesis of V. cholerae .
    Type of Medium: Online Resource
    ISSN: 0099-2240 , 1098-5336
    RVK:
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2021
    detail.hit.zdb_id: 223011-2
    detail.hit.zdb_id: 1478346-0
    SSG: 12
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  • 3
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 119, No. 11 ( 2022-03-15)
    Abstract: Members of complex microbial communities that reside in environments such as the mammalian gut have evolved mechanisms of interspecies competition, which may be directed at resident microbial and host cells. While previous work has focused mainly on metabolic or niche competition, few specific intermicrobial targeting mechanisms have been elucidated in the mammalian gut. Here, we show that a genotoxin produced by commensal Escherichia coli , colibactin, which was previously shown to induce DNA damage in host intestinal cells, is also able to target via a contact-dependent mechanism a variety of enteric pathogens and commensals, including the important human diarrheal pathogen Vibrio cholerae . We find that colibactin-mediated killing depends on accumulation of intracellular reactive oxygen species, leading to DNA damage and loss of target cell fitness. We also show that the presence of colibactin is associated with cholera outcomes in a large human metagenomic dataset and that colibactin can shape the microbiome by species-specific targeting of a common human gut-associated microbe Bacteroides fragilis , suggesting that genotoxin-mediated mechanisms may have broad effects in the complex polymicrobial interactions that shape commensal microbial communities and their effects on host health and disease.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    RVK:
    RVK:
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2022
    detail.hit.zdb_id: 209104-5
    detail.hit.zdb_id: 1461794-8
    SSG: 11
    SSG: 12
    Location Call Number Limitation Availability
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