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. 2021 Feb 17;12:25. doi: 10.1186/s40104-020-00532-4

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© The Author(s) 2021

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 8 — Proposed mechanism of LrEVs-mediated bacteria-host crosstalk to drive the intestinal immune homeostasis against pathogens-induced inflammation in the chicken model. In inflammatory bowel disease, pathogens remarkably proliferate in the gut lumen and produce pro-inflammatory signals, such as lipopolysaccharide (LPS), which activate inflammatory cells, including macrophages (Mφ), Th1 and Th17 cells, to produce pro-inflammatory responses (1) [57]. L. reuteri BBC3 releases nanosized and highly biocompatible EVs that can drive the long-distance transport of interior molecules throughout the intracellular compartments in a concentrated, protected and targeted manner (2) [72]. These vesicles can suppress the pro-inflammatory mediators produced by inflammatory cells (activated Mφ) (3), and activate innate immune cells, including naïve Mφ (4) and possibly dendritic cells (DCs) (5), to produce immunoregulatory cytokines (possibly including IL-10) (6) that induce the development of immunoregulatory CD4⁺CD25⁺ cells. These resulting CD4⁺CD25⁺ cells can produce anti-inflammatory cytokines IL-10 and TGF-β that inhibit the production of pro-inflammatory cytokines (7) [62]. Further studies are required to investigate the potential interactions between LrEVs and other intestinal immune cells, especially DCs (5) and epithelial cells (8)