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      Plant-Derived Exosomal MicroRNAs Shape the Gut Microbiota

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          Abstract

          <p id="P3">The gut microbiota can be altered by dietary interventions to prevent and treat various diseases. However, the mechanisms by which food products modulate commensals remain largely unknown. We demonstrate that plant-derived <span style="text-decoration: underline">e</span>xosomes- <span style="text-decoration: underline">l</span>ike <span style="text-decoration: underline">n</span>anoparticles (ELNs) are taken up by the gut microbiota and contain RNAs that alter microbiome composition and host physiology. Ginger ELNs (GELNs) are preferentially taken up by <i>Lactobacillaceae</i> in a GELN lipid-dependent manner and contain microRNAs that target various genes in Lactobacillus rhamnosus (LGG). Among these, GELN mdo-miR7267-3p-mediated targeting of the LGG monooxygenase ycnE yields increased indole-3-carboxaldehyde (I3A). GELN RNAs or I3A, a ligand for aryl hydrocarbon receptor (AHR), are sufficient to induce production of IL-22, which is linked to barrier function improvement. These functions of GELN RNAs can ameliorate mouse colitis via IL-22-dependent mechanisms. These findings reveal how plant products and their effects on the microbiome may be used to target specific host processes to alleviate disease. </p><p id="P4"> <div class="figure-container so-text-align-c"> <img alt="" class="figure" src="/document_file/0d10b54b-b4a1-4c0a-9924-cb15ee796b08/PubMedCentral/image/nihms-1509217-f0001.jpg"/> </div> </p><p class="first" id="P5">Teng et al. show that exosomes-like nanoparticles (ELNs) from edible plants such as ginger are preferentially taken up by gut bacteria in an ELN lipid dependent manner. ELN RNAs regulate gut microbiota composition and localization as well as host physiology, notably enhancing gut barrier function to alleviate colitis. </p>

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          Author and article information

          Journal
          Cell Host & Microbe
          Cell Host & Microbe
          Elsevier BV
          19313128
          October 2018
          October 2018
          Article
          10.1016/j.chom.2018.10.001
          6746408
          30449315
          f4f6d0ed-a911-4cb4-ab71-b25a05fdb91c
          © 2018

          https://www.elsevier.com/tdm/userlicense/1.0/

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