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. 2019 Oct 10;9:14661. doi: 10.1038/s41598-019-51092-1

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© The Author(s) 2019

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Putative and confirmed mechanisms through which milk EVs modulate inflammation. A20 plays a central role in regulating inflammation through the NFκB pathway. Milk EVs regulate A20 expression with P100K EVs specifically downregulating A20-inhibitor miR-125b. Black arrows represent previously reported interactions. Green arrows represent the new findings unveiled by the present study. More details are available in the discussion of this report. The bioactive compounds of milk EVs responsible for their bioactivity are yet to clarify, as is the mechanism ensuring their release in the cytoplasm. *Certain EV subset might be more potent than the others in the specified interaction. Abbreviations. EVs, extracellular vesicles; P100K, pellet 100,000 g; P35K, pellet 35,000 g. Made with BioRender.com.