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. 2019 Oct 1;10:2155. doi: 10.3389/fmicb.2019.02155

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Copyright © 2019 Ashrafian, Shahriary, Behrouzi, Moradi, Keshavarz Azizi Raftar, Lari, Hadifar, Yaghoubfar, Ahmadi Badi, Khatami, Vaziri and Siadat.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Administration of A. muciniphila and its EVs improves the intestinal and metabolic homeostasis in obese mice. Obesity is associated with the disruption of the intestinal barrier integrity, inflammation, and fat mass gain (left). Oral administration of A. muciniphila or its EVs increase the expression of tight junction proteins and TLR-2 and reduce the expression of TLR-4 and pro-inflammatory cytokines in the colon of obese mice (right). Also, treatment with A. muciniphila and its EVs affects FA oxidation, local inflammation genes, and fat-mass loss in the EAT of obese mice. HFD, high-fat diet; EVs, extracellular vesicles; TLR, toll-like receptor; LPS, lipopolysaccharide; PPAR, peroxisome proliferator-activated receptor; Zo-1, zonula occludens-1; Ocldn, occludin; Cldn, claudin; Angptl4, angiopoietin-like 4; TNF-α, tumor necrosis factor-α; IL-10, interleukin-10; TGF-β, transforming growth factor-β; and Glc, glucose.