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L-Tryptophan represses persister formation via inhibiting bacterial motility and promoting antibiotics absorption

    Yan Li

    *Author for correspondence: Tel.: +86 531 8838 2042;

    E-mail Address: liyan2015@sdu.edu.cn

    Department of Pathogen Biology, School of Basic Medical Science, Shandong University, Jinan, China

    ,
    Bo Liu

    Shanghai Pudong New Area Center for Disease Control & Prevention, Shanghai, China

    ,
    Jingjing Guo

    Department of Pathogen Biology, School of Basic Medical Science, Shandong University, Jinan, China

    ,
    Hua Cong

    Department of Pathogen Biology, School of Basic Medical Science, Shandong University, Jinan, China

    ,
    Shenyi He

    Department of Pathogen Biology, School of Basic Medical Science, Shandong University, Jinan, China

    ,
    Huaiyu Zhou

    Department of Pathogen Biology, School of Basic Medical Science, Shandong University, Jinan, China

    ,
    Faliang Zhu

    Department of Immunology, School of Basic Medical Science, Shandong University, Jinan, China

    ,
    Qun Wang

    Department of Immunology, School of Basic Medical Science, Shandong University, Jinan, China

    &
    Lining Zhang

    Department of Immunology, School of Basic Medical Science, Shandong University, Jinan, China

    Published Online:https://doi.org/10.2217/fmb-2019-0051

    Aim: The bacterial persisters have emerged as a huge threat to human health. Here, we investigated the role of L-tryptophan in bacterial persister killing by aminoglycoside antibiotics (AGs). Materials & methods: The relevance to the antibiotic susceptibility of Escherichia coli including transcriptional sequencing, gene expression, intracellular ATP, Nicotinamide adenine dinucleotide (NAD/NADH), reactive oxygen species and membrane depolarization were determined. Results & conclusion: We found that exogenous L-tryptophan efficiently inhibited AGs-enabled persisters. The flagellar genes were almost significantly downregulated. Besides, the AGs uptake was obviously increased as the result of elevation in proton motive force (PMF) in response to L-tryptophan-mediated NADH production. Taken together, these data supported a novel role of L-tryptophan in eradicating AGs persisters against E. coli.

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