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. 2017 Jul 5;11:191. doi: 10.3389/fncel.2017.00191

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Copyright © 2017 McMillin, Frampton, Grant, Khan, Diocares, Petrescu, Wyatt, Kain, Jefferson and DeMorrow.

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) or licensor 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 of S1PR2-mediated neuroinflammation during AOM-induced HE. AOM-induced liver failure disrupts the enterohepatic circulation and causes hepatocyte death leading to an increase of circulating bile acids including TCA. TCA crosses the leaky blood brain barrier and binds S1PR2 in neurons. This leads to increased expression and secretion of CCL2 from neurons, which binds receptors on microglia leading to their activation. This ultimately results in increased proinflammatory cytokine expression and worse HE outcomes.