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. 2022 May 19;16:876582. doi: 10.3389/fnins.2022.876582

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Copyright © 2022 Chen, Bai, Dilimulati, Shao, Qiu, Liu, Xu, Bai, Du, Zhou, Lin, Meng, Jin, Liu, Zhang, Duan and Jia.

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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Working model for the exacerbation of ischemic stroke by periodontitis salivary microbiota. Periodontitis salivary microbiota increases IL-17A-producing cells in the small intestine, which contain CD4⁺ T cells and TCR-γδ⁺ T cells. Increased migration of IL-17A-producing cells from the gut to the brain elevates post-ischemic chemokines (Cxcl1, Cxcl2, and Ccl2) and ultimately infiltration and activation of immune cells (macrophages/microglia, astrocyte, and neutrophils) in ischemic brain, leading to exacerbated neuroinflammation and ischemic stroke phenotype.