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. Author manuscript; available in PMC: 2020 Aug 1.
Published in final edited form as: Stroke. 2019 Jul 5;50(8):2270–2277. doi: 10.1161/STROKEAHA.119.025140

Figure 3. Effects of stroke on the microbiota-gut-brain axis.

Figure 3.

A) Alterations to the gut and microbiota following stroke includes loss of enteric nerves, epithelial barrier breakdown, translocation of bacteria and bacterial toxins, loss of goblet cells, thinning of the mucus barrier, and gut dysbiosis. B) Two proposed mechanisms of gut immune cell activation and tracking to brain following stroke. (a) Following stroke, a pro-inflammatory microbiota leads to increased TH1 cells, TH17 cells and monocytes in Peyer’s Patches in the small intestine. (b) T cells, TH cells and monocytes migrate from Peyer’s Patches to the peri-infarct region. (c) In the presence of a pro-inflammatory microbiota, dendritic cells migrate to mesenteric lymph nodes to inhibit polarization of T cells into anti-inflammatory T reg cells. (d) In turn, decreased T reg cells migrating to the lamina propria favors γδ T cell differentiation. (e) Pro-inflammatory γδ T cells originating from the lamina propria of the small intestine migrate to the meninges and increase infarct size.