Degradation of trimethylamine in vitro and in vivo by Enterococcus faecalis isolated from healthy human gut.

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Title: Degradation of trimethylamine in vitro and in vivo by Enterococcus faecalis isolated from healthy human gut.
Authors: Chen, Yi-ran1,2, Fang, Shu-ting1, Liu, Hai-yue2, Zheng, Hui-min1,2, He, Yan2, Chen, Ze-wei3, Chen, Mu-xuan2, Zhang, Guo-xia1 guoxiazhang@126.com, Zhou, Hong-wei1,2 biodegradation@gmail.com
Source: International Biodeterioration & Biodegradation. Nov2018, Vol. 135, p24-32. 9p.
Subjects: Biodegradation, Trimethylamine, Enterococcus faecalis, Gut microbiota, Choline, Trimethylamine oxide, Cardiovascular diseases
Abstract: Abstract Gut microbes are capable of transforming choline into trimethylamine (TMA), and elevated serum trimethylamine- N -oxide (TMAO) levels are associated with cardiovascular diseases. Therapeutic approaches have focused on inhibiting microbial TMA formation. However, little is known about the degradation of TMA by gut bacteria. Here, we anaerobically cultivated and analyzed communities cultured with or without TMA. Enterococcus was significantly more abundant in communities cultured with TMA. Based on this observation, six Enterococcus strains were isolated from healthy human faecal samples, of which 3 Enterococcus faecalis isolates (E. faecalis Ef1, E. faecalis Ef2 and E. faecalis Ef3) could enable TMA degradation anaerobically. We further tested whether increased plasma TMAO levels in rats induced by a TMA-laden diet were attenuated by the administration of TMA-degrading E. faecalis. The results showed that these strains attenuated TMAO levels (mean 405.741 ng mL−1 for the experimental group vs mean 513.96 ng mL−1 for the control group, p < 0.05) after 14 days' administration. To the best of our knowledge, our report is the first to demonstrate the TMA-degrading ability of human gut bacteria in vitro and in vivo. These results provide new insights into the prevention of TMAO-induced cardiovascular disease and suggest novel therapeutic approaches. Highlights • Human gut Enterococcus faecalis enables trimethylamine degradation anaerobically. • Trimethylamine-degrading E. faecalis reduced rats serum trimethylamine- N -oxide levels. • First report on trimethylamine degradation by human gut bacteria ex vivo and in vivo. [ABSTRACT FROM AUTHOR]
Copyright of International Biodeterioration & Biodegradation is the property of Elsevier B.V. and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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  Data: Degradation of trimethylamine in vitro and in vivo by Enterococcus faecalis isolated from healthy human gut.
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  Data: Abstract Gut microbes are capable of transforming choline into trimethylamine (TMA), and elevated serum trimethylamine- N -oxide (TMAO) levels are associated with cardiovascular diseases. Therapeutic approaches have focused on inhibiting microbial TMA formation. However, little is known about the degradation of TMA by gut bacteria. Here, we anaerobically cultivated and analyzed communities cultured with or without TMA. Enterococcus was significantly more abundant in communities cultured with TMA. Based on this observation, six Enterococcus strains were isolated from healthy human faecal samples, of which 3 Enterococcus faecalis isolates (E. faecalis Ef1, E. faecalis Ef2 and E. faecalis Ef3) could enable TMA degradation anaerobically. We further tested whether increased plasma TMAO levels in rats induced by a TMA-laden diet were attenuated by the administration of TMA-degrading E. faecalis. The results showed that these strains attenuated TMAO levels (mean 405.741 ng mL−1 for the experimental group vs mean 513.96 ng mL−1 for the control group, p &lt; 0.05) after 14 days&#39; administration. To the best of our knowledge, our report is the first to demonstrate the TMA-degrading ability of human gut bacteria in vitro and in vivo. These results provide new insights into the prevention of TMAO-induced cardiovascular disease and suggest novel therapeutic approaches. Highlights • Human gut Enterococcus faecalis enables trimethylamine degradation anaerobically. • Trimethylamine-degrading E. faecalis reduced rats serum trimethylamine- N -oxide levels. • First report on trimethylamine degradation by human gut bacteria ex vivo and in vivo. [ABSTRACT FROM AUTHOR]
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  Data: &lt;i&gt;Copyright of International Biodeterioration &amp; Biodegradation is the property of Elsevier B.V. and its content may not be copied or emailed to multiple sites without the copyright holder&#39;s express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.&lt;/i&gt; (Copyright applies to all Abstracts.)
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      – Type: doi
        Value: 10.1016/j.ibiod.2018.09.005
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        Text: English
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      Pagination:
        PageCount: 9
        StartPage: 24
    Subjects:
      – SubjectFull: Biodegradation
        Type: general
      – SubjectFull: Trimethylamine
        Type: general
      – SubjectFull: Enterococcus faecalis
        Type: general
      – SubjectFull: Gut microbiota
        Type: general
      – SubjectFull: Choline
        Type: general
      – SubjectFull: Trimethylamine oxide
        Type: general
      – SubjectFull: Cardiovascular diseases
        Type: general
    Titles:
      – TitleFull: Degradation of trimethylamine in vitro and in vivo by Enterococcus faecalis isolated from healthy human gut.
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              M: 11
              Text: Nov2018
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              Y: 2018
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